Liver Cancer

Overview

Literature Analysis

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Tag cloud generated 29 August, 2019 using data from PubMed, MeSH and CancerIndex

Mutated Genes and Abnormal Protein Expression (415)

How to use this data tableClicking on the Gene or Topic will take you to a separate more detailed page. Sort this list by clicking on a column heading e.g. 'Gene' or 'Topic'.

GeneLocationAliasesNotesTopicPapers
HCCS Xp22.2 MLS, CCHL, MCOPS7, LSDMCA1 -HCCS and Hepatocellular Carcinoma
1085
TP53 17p13.1 P53, BCC7, LFS1, TRP53 -TP53 and Liver Cancer
691
CTNNB1 3p22.1 CTNNB, MRD19, armadillo -CTNNB1 and Liver Cancer
514
MET 7q31.2 HGFR, AUTS9, RCCP2, c-Met, DFNB97 Prognostic
-C-MET and Liver Cancer
-C-MET and Hepatocellular Carcinoma
261
GPC3 Xq26.2 SGB, DGSX, MXR7, SDYS, SGBS, OCI-5, SGBS1, GTR2-2 -GPC3 and Liver Cancer
484
AFP 4q13.3 AFPD, FETA, HPAFP -AFP and Hepatocellular Carcinoma
430
TNF 6p21.33 DIF, TNFA, TNFSF2, TNLG1F, TNF-alpha -TNF and Liver Cancer
186
BAX 19q13.33 BCL2L4 -BAX and Liver Cancer
149
STAT3 17q21.2 APRF, HIES, ADMIO, ADMIO1 -STAT3 and Liver Cancer
135
MMP2 16q12.2 CLG4, MONA, CLG4A, MMP-2, TBE-1, MMP-II -MMP2 and Liver Cancer
114
PCNA 20p12.3 ATLD2 -PCNA and Liver Cancer
113
CDKN1A 6p21.2 P21, CIP1, SDI1, WAF1, CAP20, CDKN1, MDA-6, p21CIP1 -CDKN1A and Hepatocellular Carcinoma
112
HIF1A 14q23.2 HIF1, MOP1, PASD8, HIF-1A, bHLHe78, HIF-1alpha, HIF1-ALPHA, HIF-1-alpha -HIF1A and Liver Cancer
109
SRC 20q11.23 ASV, SRC1, THC6, c-SRC, p60-Src -SRC and Liver Cancer
102
IGF2 11p15.5 GRDF, IGF-II, PP9974, C11orf43 -IGF2 and Hepatoblastoma
-IGF2 Expression in Hepatocarcinoma
76
MYC 8q24.21 MRTL, MYCC, c-Myc, bHLHe39 -MYC protein, human and Liver Cancer
98
TERT 5p15.33 TP2, TRT, CMM9, EST2, TCS1, hTRT, DKCA2, DKCB4, hEST2, PFBMFT1 -TERT and Liver Cancer
96
TGFB1 19q13.2 CED, LAP, DPD1, TGFB, TGFbeta -TGFB1 and Liver Cancer
87
HGF 7q21.11 SF, HGFB, HPTA, F-TCF, DFNB39 -HGF and Liver Cancer
85
VEGFA 6p21.1 VPF, VEGF, MVCD1 -VEGFA and Liver Cancer
80
FOS 14q24.3 p55, AP-1, C-FOS -FOS and Liver Cancer
76
HNF1A 12q24.31 HNF1, LFB1, TCF1, MODY3, TCF-1, HNF-1A, IDDM20 -HNF1A and Liver Cancer
74
E2F1 20q11.22 RBP3, E2F-1, RBAP1, RBBP3 -E2F1 and Liver Cancer
70
IGF2R 6q25.3 MPR1, MPRI, CD222, CIMPR, M6P-R, MPR300, CI-M6PR, MPR 300, M6P/IGF2R -IGF2R and Liver Cancer
69
ABCC1 16p13.11 MRP, ABCC, GS-X, MRP1, ABC29 -ABCC1 (MRP1) and Hepatocellular Carcinoma
61
CDH1 16q22.1 UVO, CDHE, ECAD, LCAM, Arc-1, CD324 -CDH1 and Liver Cancer
60
SMAD3 15q22.33 LDS3, LDS1C, MADH3, JV15-2, HSPC193, HsT17436 -SMAD3 and Liver Cancer
59
MIR21 17q23.1 MIRN21, miR-21, miRNA21, hsa-mir-21 -MicroRNA miR-21 and Liver Cancer
54
RASSF1 3p21.31 123F2, RDA32, NORE2A, RASSF1A, REH3P21 -RASSF1 and Liver Cancer
48
SNAI1 20q13.13 SNA, SNAH, SNAIL, SLUGH2, SNAIL1, dJ710H13.1 -SNAI1 and Liver Cancer
48
HLF 17q22 -HLF and Hepatocellular Carcinoma
47
SMAD4 18q21.2 JIP, DPC4, MADH4, MYHRS -SMAD4 and Liver Cancer
47
HNF4A 20q13.12 TCF, HNF4, MODY, FRTS4, MODY1, NR2A1, TCF14, HNF4a7, HNF4a8, HNF4a9, NR2A21, HNF4alpha -HNF4A and Liver Cancer
44
TGFA 2p13 TFGA -TGFA and Liver Cancer
42
XRCC1 19q13.31 RCC -XRCC1 and Liver Cancer
41
HFE 6p22.2 HH, HFE1, HLA-H, MVCD7, TFQTL2 -HFE and Liver Cancer
41
DNMT1 19p13.2 AIM, DNMT, MCMT, CXXC9, HSN1E, ADCADN, m.HsaI -DNMT1 and Liver Cancer
41
CCNB1 5q13.2 CCNB -CCNB1 and Hepatocellular Carcinoma
40
CCK 3p22.1 -CCK and Liver Cancer
39
IL6 7p15.3 CDF, HGF, HSF, BSF2, IL-6, BSF-2, IFNB2, IFN-beta-2 -IL6 and Hepatocellular Carcinoma
39
ACHE 7q22.1 YT, ACEE, ARACHE, N-ACHE -ACHE and Liver Cancer
36
TCF4 18q21.2 E2-2, ITF2, PTHS, SEF2, FECD3, ITF-2, SEF-2, TCF-4, SEF2-1, SEF2-1A, SEF2-1B, SEF2-1D, bHLHb19 -TCF4 and Liver Cancer
36
RHOA 3p21.31 ARHA, ARH12, RHO12, RHOH12 -RHOA and Liver Cancer
36
FOXM1 12p13 MPP2, TGT3, HFH11, HNF-3, INS-1, MPP-2, PIG29, FKHL16, FOXM1B, HFH-11, TRIDENT, MPHOSPH2 -FOXM1 and Liver Cancer
34
GAPDH 12p13.31 G3PD, GAPD, HEL-S-162eP -GAPDH and Liver Cancer
33
GSTT1 22q11.23 -GSTT1 and Liver Cancer
32
XIAP Xq25 API3, ILP1, MIHA, XLP2, BIRC4, IAP-3, hIAP3, hIAP-3 -XIAP and Liver Cancer
31
RUNX3 1p36.11 AML2, CBFA3, PEBP2aC -RUNX3 and Liver Cancer
31
RHOC 1p13.2 H9, ARH9, ARHC, RHOH9 -RHOC and Liver Cancer
31
AXIN1 16p13.3 AXIN, PPP1R49 -AXIN1 and Liver Cancer
30
IFNL3 19q13.2 IL28B, IL28C, IL-28B, IL-28C, IFN-lambda-3, IFN-lambda-4 -IL28B and Liver Cancer
30
ARID1A 1p36.11 ELD, B120, CSS2, OSA1, P270, hELD, BM029, MRD14, hOSA1, BAF250, C1orf4, BAF250a, SMARCF1 -ARID1A and Liver Cancer
30
M6PR 12p13 SMPR, MPR46, CD-MPR, MPR 46, MPR-46 -M6PR and Liver Cancer
29
SOCS1 16p13.13 JAB, CIS1, SSI1, TIP3, CISH1, SSI-1, SOCS-1 -SOCS1 and Liver Cancer
29
SPP1 4q22.1 OPN, BNSP, BSPI, ETA-1 -SPP1 and Liver Cancer
29
MTDH 8q22.1 3D3, AEG1, AEG-1, LYRIC, LYRIC/3D3 -MTDH and Liver Cancer
29
SIRT1 10q21.3 SIR2, SIR2L1, SIR2alpha -SIRT1 and Liver Cancer
28
BAD 11q13.1 BBC2, BCL2L8 -BAD and Liver Cancer
28
DNMT3B 20q11.21 ICF, ICF1, M.HsaIIIB -DNMT3B and Liver Cancer
28
JUNB 19p13.13 AP-1 -JUNB and Hepatocellular Carcinoma
27
PTK2 8q24.3 FAK, FADK, FAK1, FRNK, PPP1R71, p125FAK, pp125FAK -PTK2 and Liver Cancer
27
VIP 6q25.2 PHM27 -VIP and Liver Cancer
26
KLF6 10p15.2 GBF, ZF9, BCD1, CBA1, CPBP, PAC1, ST12, COPEB -KLF6 and Liver Cancer
26
IGFBP3 7p12.3 IBP3, BP-53 -IGFBP3 and Liver Cancer
26
YAP1 11q22.1 YAP, YKI, COB1, YAP2, YAP65 -YAP1 and Liver Cancer
25
MICA 6p21.33 MIC-A, PERB11.1 -MICA and Liver Cancer
25
DLC1 8p22 HP, ARHGAP7, STARD12, p122-RhoGAP Deletion
-DLC1 and Hepatocellular Carcinoma
25
EPCAM 2p21 ESA, KSA, M4S1, MK-1, DIAR5, EGP-2, EGP40, KS1/4, MIC18, TROP1, EGP314, HNPCC8, TACSTD1 -EPCAM and Liver Cancer
24
RAC1 7p22.1 MIG5, Rac-1, TC-25, p21-Rac1 -RAC1 and Hepatocellular Carcinoma
23
ANGPT2 8p23.1 ANG2, AGPT2 -ANGPT2 and Liver Cancer
23
CDC42 1p36.12 TKS, G25K, CDC42Hs -CDC42 and Liver Cancer
23
FTCDNL1 2q33.1 FONG -FONG and Liver Cancer
22
BECN1 17q21.31 ATG6, VPS30, beclin1 -BECN1 and Liver Cancer
21
MAGEA1 Xq28 CT1.1, MAGE1 -MAGEA1 and Hepatocellular Carcinoma
20
CCL2 17q12 HC11, MCAF, MCP1, MCP-1, SCYA2, GDCF-2, SMC-CF, HSMCR30 -CCL2 and Hepatocellular Carcinoma
19
HMGB1 13q12.3 HMG1, HMG3, HMG-1, SBP-1 -HMGB1 and Liver Cancer
19
SFRP1 8p11.21 FRP, FRP1, FrzA, FRP-1, SARP2 -SFRP1 and Hepatocellular Carcinoma
18
MAT1A 10q22.3 MAT, SAMS, MATA1, SAMS1 -MAT1A and Liver Cancer
18
YY1AP1 1q22 GRNG, HCCA1, HCCA2, YY1AP -YY1AP1 and Liver Cancer
18
APOB 2p24-p23 FLDB, LDLCQ4 -APOB and Liver Cancer
17
TIMP3 22q12.3 SFD, K222, K222TA2, HSMRK222 -TIMP3 and Liver Cancer
17
TCF7L2 10q25.2-q25.3 TCF4, TCF-4 -TCF7L2 and Liver Cancer
17
KIF1B 1p36.22 KLP, CMT2, CMT2A, CMT2A1, HMSNII, NBLST1 -KIF1B and Liver Cancer
16
PDCD4 10q25.2 H731 -PDCD4 and Liver Cancer
16
HNF1B 17q12 FJHN, HNF2, LFB3, TCF2, HPC11, LF-B3, MODY5, TCF-2, VHNF1, HNF-1B, HNF1beta, HNF-1-beta -HNF1B and Liver Cancer
16
IL6ST 5q11.2 CD130, GP130, CDW130, IL-6RB -IL6ST and Liver Cancer
16
JAG1 20p12.2 AGS, AHD, AWS, HJ1, AGS1, DCHE, CD339, JAGL1 -JAG1 and Liver Cancer
16
FASN 17q25.3 FAS, OA-519, SDR27X1 -FASN and Liver Cancer
16
NFKBIA 14q13.2 IKBA, MAD-3, NFKBI -NFKBIA and Liver Cancer
16
MALAT1 11q13.1 HCN, NEAT2, PRO2853, LINC00047, NCRNA00047 -MALAT1 and Liver Cancer
15
TNFRSF1A 12p13.31 FPF, p55, p60, TBP1, TNF-R, TNFAR, TNFR1, p55-R, CD120a, TNFR55, TNFR60, TNF-R-I, TNF-R55 -TNFRSF1A and Hepatocellular Carcinoma
15
CCNE1 19q12 CCNE, pCCNE1 -CCNE1 and Liver Cancer
15
FOXA2 20p11.21 HNF3B, TCF3B -FOXA2 and Liver Cancer
15
PSMD10 Xq22.3 p28, p28(GANK), dJ889N15.2 -PSMD10 and Liver Cancer
15
MIRLET7C 21q21.1 LET7C, let-7c, MIRNLET7C, hsa-let-7c -MicroRNA let-7c and Liver Cancer
15
PEG10 7q21.3 EDR, HB-1, Mar2, MEF3L, Mart2, RGAG3 -PEG10 and Hepatocellular Carcinoma
15
PLK1 16p12.2 PLK, STPK13 -PLK1 and Liver Cancer
15
WNT3A 1q42.13 -WNT3A and Liver Cancer
14
NFE2L2 2q31 NRF2 -NFE2L2 and Liver Cancer
14
MAGEA3 Xq28 HIP8, HYPD, CT1.3, MAGE3, MAGEA6 -MAGEA3 and Hepatocellular Carcinoma
14
ANXA2 15q22.2 P36, ANX2, LIP2, LPC2, CAL1H, LPC2D, ANX2L4, PAP-IV, HEL-S-270 -ANXA2 and Hepatocellular Carcinoma
14
HEBP1 12p13.1 HBP, HEBP -HEBP1 and Liver Cancer
14
SREBF1 17p11.2 SREBP1, bHLHd1, SREBP1a, SREBP-1c -SREBF1 and Liver Cancer
14
GNMT 6p12 -GNMT and Liver Cancer
14
FGF19 11q13.3 -FGF19 and Hepatocellular Carcinoma
13
RECK 9p13.3 ST15 -RECK and Liver Cancer
13
HES1 3q29 HHL, HRY, HES-1, bHLHb39 -HES1 and Liver Cancer
13
AXIN2 17q24.1 AXIL, ODCRCS -AXIN2 and Liver Cancer
13
DDX3X Xp11.4 DBX, DDX3, HLP2, DDX14, CAP-Rf, MRX102 -DDX3X and Liver Cancer
12
SALL4 20q13.2 DRRS, HSAL4, ZNF797 -SALL4 and Liver Cancer
12
ZEB2 2q22.3 SIP1, SIP-1, ZFHX1B, HSPC082, SMADIP1 -ZEB2 and Liver Cancer
12
DKK1 10q21.1 SK, DKK-1 -DKK1 and Hepatocellular Carcinoma
12
CCL4 17q12 ACT2, G-26, HC21, LAG1, LAG-1, MIP1B, SCYA2, SCYA4, MIP1B1, AT744.1, MIP-1-beta -CCL4 and Hepatocellular Carcinoma
12
CDC20 1p34.2 CDC20A, p55CDC, bA276H19.3 -CDC20 and Liver Cancer
12
MACC1 7p21.1 7A5, SH3BP4L -MACC1 and Liver Cancer
12
STMN1 1p36.11 Lag, SMN, OP18, PP17, PP19, PR22, LAP18, C1orf215 -STMN1 and Liver Cancer
11
AKR1B10 7q33 HIS, HSI, ARL1, ARL-1, ALDRLn, AKR1B11, AKR1B12 -AKR1B10 and Liver Cancer
11
DLK1 14q32.2 DLK, FA1, ZOG, pG2, DLK-1, PREF1, Delta1, Pref-1 -DLK1 and Liver Cancer
11
ARID2 12q12 p200, BAF200 -ARID2 and Liver Cancer
11
VIM 10p13 HEL113, CTRCT30 -VIM and Liver Cancer
11
ADAM10 15q21.3 RAK, kuz, AD10, AD18, MADM, CD156c, CDw156, HsT18717 -ADAM10 and Liver Cancer
11
KEAP1 19p13.2 INrf2, KLHL19 -KEAP1 and Hepatocellular Carcinoma
11
APOE 19q13.32 AD2, LPG, APO-E, ApoE4, LDLCQ5 -APOE and Hepatocellular Carcinoma
11
SMYD3 1q44 KMT3E, ZMYND1, ZNFN3A1, bA74P14.1 -SMYD3 and Liver Cancer
11
PIN1 19p13.2 DOD, UBL5 -PIN1 and Hepatocellular Carcinoma
11
HDAC3 5q31.3 HD3, RPD3, RPD3-2 -HDAC3 and Hepatocellular Carcinoma
10
ING1 13q34 p33, p47, p33ING1, p24ING1c, p33ING1b, p47ING1a -ING1 and Hepatocellular Carcinoma
10
HDGF 1q23.1 HMG1L2 -HDGF and Liver Cancer
10
FYN 6q21 SLK, SYN, p59-FYN -FYN and Liver Cancer
10
ACTB 7p22.1 BRWS1, PS1TP5BP1 -ACTB and Hepatocellular Carcinoma
10
CXCL10 4q21.1 C7, IFI10, INP10, IP-10, crg-2, mob-1, SCYB10, gIP-10 -CXCL10 and Liver Cancer
10
TLR3 4q35.1 CD283, IIAE2 -TLR3 and Liver Cancer
10
GPX1 3p21.31 GPXD, GSHPX1 -GPX1 and Liver Cancer
10
CYP2C19 10q23.33 CPCJ, CYP2C, P450C2C, CYPIIC17, CYPIIC19, P450IIC19 -CYP2C19 and Liver Cancer
10
CCR7 17q21.2 BLR2, EBI1, CCR-7, CD197, CDw197, CMKBR7, CC-CKR-7 -CCR7 and Liver Cancer
10
NEK2 1q32.3 NLK1, RP67, NEK2A, HsPK21, PPP1R111 -NEK2 and Liver Cancer
10
ATG5 6q21 ASP, APG5, APG5L, hAPG5, APG5-LIKE -ATG5 and Hepatocellular Carcinoma
10
TLR2 4q31.3 TIL4, CD282 -TLR2 and Liver Cancer
9
MIR107 10q23.31 MIRN107, miR-107 -MIRN107 microRNA, human and Liver Cancer
9
PTTG1 5q33.3 EAP1, PTTG, HPTTG, TUTR1 -PTTG1 and Liver Cancer
9
NDRG1 8q24.22 GC4, RTP, DRG1, NDR1, NMSL, TDD5, CAP43, CMT4D, DRG-1, HMSNL, RIT42, TARG1, PROXY1 -NDRG1 and Hepatocellular Carcinoma
9
PTP4A3 8q24.3 PRL3, PRL-3, PRL-R -PTP4A3 and Liver Cancer
9
PRDM2 1p36.21 RIZ, KMT8, RIZ1, RIZ2, KMT8A, MTB-ZF, HUMHOXY1 -PRDM2 and Liver Cancer
9
SPINK1 5q32 TCP, PCTT, PSTI, TATI, Spink3 -SPINK1 and Liver Cancer
9
AREG 4q13.3 AR, SDGF, AREGB, CRDGF -AREG and Liver Cancer
9
XBP1 22q12.1 XBP2, TREB5, XBP-1, TREB-5 -XBP1 and Liver Cancer
9
SOCS3 17q25.3 CIS3, SSI3, ATOD4, Cish3, SSI-3, SOCS-3 -SOCS3 and Liver Cancer
9
CCNG1 5q34 CCNG -CCNG1 and Liver Cancer
9
MIR122 18q21.31 MIR122A, MIRN122, mir-122, MIRN122A, miRNA122, miRNA122A, hsa-mir-122 -MIR122 and Liver Cancer
9
AGO2 8q24.3 PPD, Q10, CASC7, EIF2C2, LINC00980 -EIF2C2 and Hepatocellular Carcinoma
8
SERPINE1 7q22.1 PAI, PAI1, PAI-1, PLANH1 -SERPINE1 and Liver Cancer
8
TIMP2 17q25.3 DDC8, CSC-21K -TIMP2 and Liver Cancer
8
MEG3 14q32.2 GTL2, FP504, prebp1, PRO0518, PRO2160, LINC00023, NCRNA00023, onco-lncRNA-83 -MEG3 and Liver Cancer
8
CDH2 18q12.1 CDHN, NCAD, CD325, CDw325 -CDH2 and Liver Cancer
8
ZBTB7A 19p13.3 LRF, FBI1, FBI-1, TIP21, ZBTB7, ZNF857A, pokemon -ZBTB7A and Liver Cancer
8
YES1 18p11.32 Yes, c-yes, HsT441, P61-YES -Proto-Oncogene Proteins c-yes and Liver Cancer
8
SPINT2 19q13.2 PB, Kop, HAI2, DIAR3, HAI-2 -SPINT2 and Liver Cancer
8
ATF3 1q32.3 -ATF3 and Liver Cancer
8
PROX1 1q32.3 -PROX1 and Liver Cancer
8
LGR5 12q22-q23 FEX, HG38, GPR49, GPR67, GRP49 -LGR5 and Liver Cancer
8
MTSS1 8q24.13 MIM, MIMA, MIMB -MTSS1 and Liver Cancer
8
PIGS 17q11.2 -PIGS and Liver Cancer
8
BTG2 1q32.1 PC3, APRO1, TIS21 -BTG2 and Liver Cancer
8
SULF2 20q13.12 HSULF-2 -SULF2 and Liver Cancer
8
LIN28B 6q16.3-q21 CSDD2 -LIN28B and Liver Cancer
8
LCN2 9q34.11 p25, 24p3, MSFI, NGAL -LCN2 and Liver Cancer
8
ATF6 1q23.3 ACHM7, ATF6A -ATF6 and Liver Cancer
8
PGK1 Xq21.1 PGKA, MIG10, HEL-S-68p -PGK1 and Liver Cancer
8
HOTAIR 12q13.13 HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 -HOTAIR and Liver Cancer
8
GADD45B 19p13.3 MYD118, GADD45BETA -GADD45B and Hepatocellular Carcinoma
7
CTAG1B Xq28 CTAG, ESO1, CT6.1, CTAG1, LAGE-2, LAGE2B, NY-ESO-1 -CTAG1B and Liver Cancer
7
XIST Xq13.2 SXI1, swd66, DXS1089, DXS399E, LINC00001, NCRNA00001 -XIST and Hepatocellular Carcinoma
7
PPARGC1A 4p15.2 LEM6, PGC1, PGC1A, PGC-1v, PPARGC1, PGC-1alpha, PGC-1(alpha) -PPARGC1A and Liver Cancer
7
MICB 6p21.33 PERB11.2 -MICB and Liver Cancer
7
DUSP1 5q35.1 HVH1, MKP1, CL100, MKP-1, PTPN10 -DUSP1 and Liver Cancer
7
TCF3 19p13.3 E2A, E47, AGM8, ITF1, VDIR, TCF-3, bHLHb21 -TCF3 and Liver Cancer
7
BCL2L2 14q11.2 BCLW, BCL-W, PPP1R51, BCL2-L-2 -BCL2L2 and Liver Cancer
7
IQGAP1 15q26.1 SAR1, p195, HUMORFA01 -IQGAP1 and Liver Cancer
7
KRT19 17q21.2 K19, CK19, K1CS -KRT19 and Liver Cancer
7
XAF1 17p13.1 BIRC4BP, XIAPAF1, HSXIAPAF1 -XAF1 and Liver Cancer
7
USF1 1q23.3 UEF, FCHL, MLTF, FCHL1, MLTFI, HYPLIP1, bHLHb11 -USF1 and Liver Cancer
7
LAPTM4B 8q22.1 LC27, LAPTM4beta -LAPTM4B and Liver Cancer
7
ADH1B 4q23 ADH2, HEL-S-117 -ADH1B and Hepatocellular Carcinoma
7
CD81 11p15.5 S5.7, CVID6, TAPA1, TSPAN28 -CD81 and Liver Cancer
7
ID2 2p25 GIG8, ID2A, ID2H, bHLHb26 -ID2 Expression in hepatocellular carcinoma
7
PINX1 8p23.1 LPTL, LPTS -PINX1 and Hepatocellular Carcinoma
7
NR5A2 1q32.1 B1F, CPF, FTF, B1F2, LRH1, LRH-1, FTZ-F1, hB1F-2, FTZ-F1beta -NR5A2 and Liver Cancer
7
PER3 1p36.23 GIG13, FASPS3 -PER3 and Liver Cancer
7
PTPN6 12p13 HCP, HCPH, SHP1, SHP-1, HPTP1C, PTP-1C, SHP-1L, SH-PTP1 -PTPN6 and Liver Cancer
6
IRF2 4q35.1 IRF-2 -IRF2 and Hepatocellular Carcinoma
6
ADAM17 2p25 CSVP, TACE, NISBD, ADAM18, CD156B, NISBD1 -ADAM17 and Liver Cancer
6
SERPINA1 14q32.13 PI, A1A, AAT, PI1, A1AT, PRO2275, alpha1AT -SERPINA1 and Liver Cancer
6
LAMC2 1q25.3 B2T, CSF, EBR2, BM600, EBR2A, LAMB2T, LAMNB2 -LAMC2 and Liver Cancer
6
SFRP5 10q24.2 SARP3 -SFRP5 and Liver Cancer
6
IL12A 3q25.33 P35, CLMF, NFSK, NKSF1, IL-12A -IL12A and Liver Cancer
6
ABCA1 9q31.1 TGD, ABC1, CERP, ABC-1, HDLDT1 -ABCA1 and Liver Cancer
6
CD46 1q32.2 MCP, TLX, AHUS2, MIC10, TRA2.10 -CD46 and Liver Cancer
6
TLR7 Xp22.2 TLR7-like -TLR7 and Liver Cancer
6
SULF1 8q13.2-q13.3 SULF-1 -SULF1 and Liver Cancer
6
HSF1 8q24.3 HSTF1 -HSF1 and Liver Cancer
6
NDRG2 14q11.2 SYLD -NDRG2 and Liver Cancer
6
DGCR8 22q11.21 Gy1, pasha, DGCRK6, C22orf12 -DGCR8 and Liver Cancer
6
IGFBP7 4q12 AGM, PSF, TAF, FSTL2, IBP-7, MAC25, IGFBP-7, RAMSVPS, IGFBP-7v, IGFBPRP1 -IGFBP7 and Liver Cancer
6
ADAR 1q21.3 DSH, AGS6, G1P1, IFI4, P136, ADAR1, DRADA, DSRAD, IFI-4, K88DSRBP -ADAR and Liver Cancer
6
GDF15 19p13.11 PDF, MIC1, PLAB, MIC-1, NAG-1, PTGFB, GDF-15 -GDF15 and Liver Cancer
6
WWTR1 3q25.1 TAZ -WWTR1 and Liver Cancer
6
GSTA1 6p12.2 GST2, GTH1, GSTA1-1, GST-epsilon -GSTA1 and Hepatocellular Carcinoma
6
S100A6 1q21.3 2A9, PRA, 5B10, CABP, CACY, S10A6 -S100A6 and Liver Cancer
6
SPRY2 13q31.1 IGAN3, hSPRY2 -SPRY2 and Liver Cancer
6
SPHK1 17q25.1 SPHK -SPHK1 and Liver Cancer
6
RPS6 9p22.1 S6 -RPS6 and Liver Cancer
6
TP53BP2 1q41 BBP, 53BP2, ASPP2, P53BP2, PPP1R13A -TP53BP2 and Liver Cancer
6
IRAK1 Xq28 IRAK, pelle -IRAK1 and Hepatocellular Carcinoma
6
IL12B 5q33.3 CLMF, NKSF, CLMF2, IMD28, IMD29, NKSF2, IL-12B -IL12B and Liver Cancer
6
MIRLET7G 3p21.1 LET7G, let-7g, MIRNLET7G, hsa-let-7g -MicroRNA let-7g and Liver Cancer
6
CXCR2 2q35 CD182, IL8R2, IL8RA, IL8RB, CMKAR2, CDw128b -CXCR2 and Liver Cancer
6
PER1 17p13.1 PER, hPER, RIGUI -PER1 and Liver Cancer
6
IL6R 1q21.3 IL6Q, gp80, CD126, IL6RA, IL6RQ, IL-6RA, IL-6R-1 -IL6R and Liver Cancer
6
ANGPT1 8q23.1 AGP1, AGPT, ANG1 -ANGPT1 and Liver Cancer
6
HTATIP2 11p15.1 CC3, TIP30, SDR44U1 -HTATIP2 and Liver Cancer
6
ELAVL1 19p13.2 HUR, Hua, MelG, ELAV1 -ELAVL1 and Liver Cancer
6
LRP6 12p13.2 ADCAD2 -LRP6 and Liver Cancer
6
IGFBP1 7p12.3 AFBP, IBP1, PP12, IGF-BP25, hIGFBP-1 -IGFBP1 and Liver Cancer
6
PAK4 19q13.2 -PAK4 and Liver Cancer
6
MST1 3p21 MSP, HGFL, NF15S2, D3F15S2, DNF15S2 -MST1 and Liver Cancer
5
BCL9 1q21.2 LGS -BCL9 and Liver Cancer
5
HINT1 5q23.3 HINT, NMAN, PKCI-1, PRKCNH1 -HINT1 and Liver Cancer
5
STK4 20q13.12 KRS2, MST1, YSK3 -STK4 and Liver Cancer
5
GNA11 19p13.3 FBH, FBH2, FHH2, HHC2, GNA-11, HYPOC2 -GNA11 and Liver Cancer
5
RALGDS 9q34.13-q34.2 RGF, RGDS, RalGEF -RALGDS and Liver Cancer
5
RASSF5 1q32.1 RAPL, Maxp1, NORE1, NORE1A, NORE1B, RASSF3 -RASSF5 and Liver Cancer
5
LYVE1 11p15.4 HAR, XLKD1, LYVE-1, CRSBP-1 -LYVE1 and Liver Cancer
5
COL1A2 7q21.3 OI4 -COL1A2 and Liver Cancer
5
GAGE1 Xp11.23 CT4.1, CT4.4, GAGE4, GAGE-1, GAGE-4 -GAGE1 and Liver Cancer
5
FOSB 19q13.32 AP-1, G0S3, GOS3, GOSB -FOSB and Liver Cancer
5
TXNIP 1q21.1 THIF, VDUP1, ARRDC6, HHCPA78, EST01027 -TXNIP and Liver Cancer
5
CRY1 12q23.3 PHLL1 -CRY1 and Liver Cancer
5
ATF2 2q32 HB16, CREB2, TREB7, CREB-2, CRE-BP1 -ATF2 and Hepatocellular Carcinoma
5
CHUK 10q24.31 IKK1, IKKA, IKBKA, TCF16, NFKBIKA, IKK-alpha -CHUK and Hepatocellular Carcinoma
5
HAVCR2 5q33.3 TIM3, CD366, KIM-3, TIMD3, Tim-3, TIMD-3, HAVcr-2 -HAVCR2 and Liver Cancer
5
CRY2 11p11.2 HCRY2, PHLL2 -CRY2 and Liver Cancer
5
ANGPTL4 19p13.2 NL2, ARP4, FIAF, HARP, PGAR, HFARP, TGQTL, UNQ171, pp1158 -ANGPTL4 and Liver Cancer
5
ATG7 3p25.3 GSA7, APG7L, APG7-LIKE -ATG7 and Liver Cancer
5
SATB1 3p23 -SATB1 and Hepatocellular Carcinoma
5
FOXO4 Xq13.1 AFX, AFX1, MLLT7 -FOXO4 and Liver Cancer
5
TGFB2 1q41 LDS4, G-TSF, TGF-beta2 -TGFB2 and Liver Cancer
5
TCF7 5q31.1 TCF-1 -TCF7 and Liver Cancer
5
NR0B2 1p36.11 SHP, SHP1 -NR0B2 and Liver Cancer
5
AIFM1 Xq26.1 AIF, AUNX1, CMT2D, CMTX4, COWCK, DFNX5, NADMR, NAMSD, PDCD8, COXPD6 -AIFM1 and Liver Cancer
5
CHD5 1p36.31 CHD-5 -CHD5 and Liver Cancer
5
PRDX1 1p34.1 PAG, PAGA, PAGB, PRX1, PRXI, MSP23, NKEFA, TDPX2, NKEF-A -PRDX1 and Liver Cancer
5
BTRC 10q24.32 FWD1, FBW1A, FBXW1, bTrCP, FBXW1A, bTrCP1, betaTrCP, BETA-TRCP -BTRC and Liver Cancer
5
CKS2 9q22.2 CKSHS2 -CKS2 and Liver Cancer
5
MAGEA4 Xq28 CT1.4, MAGE4, MAGE4A, MAGE4B, MAGE-41, MAGE-X2 -MAGEA4 and Liver Cancer
5
GRASP 12q13.13 TAMALIN -GRASP and Liver Cancer
5
MCM7 7q22.1 MCM2, CDC47, P85MCM, P1CDC47, PNAS146, PPP1R104, P1.1-MCM3 -MCM7 and Liver Cancer
5
DDR1 6p21.33 CAK, DDR, NEP, HGK2, PTK3, RTK6, TRKE, CD167, EDDR1, MCK10, NTRK4, PTK3A -DDR1 and Liver Cancer
5
HLA-DQA1 6p21.32 DQ-A1, CELIAC1, HLA-DQA -HLA-DQA1 and Liver Cancer
5
UGT2B7 4q13.2 UGT2B9, UDPGTH2, UDPGT2B7, UDPGTh-2, UDPGT 2B7, UDPGT 2B9 -UGT2B7 and Liver Cancer
5
WNT3 17q21.31-q21.32 INT4, TETAMS -WNT3 and Liver Cancer
5
LDLR 19p13.2 FH, FHC, LDLCQ2 -LDLR and Liver Cancer
5
CXCL5 4q13.3 SCYB5, ENA-78 -CXCL5 and Liver Cancer
5
ADAMTS1 21q21.3 C3-C5, METH1 -ADAMTS1 and Liver Cancer
5
ADARB1 21q22.3 RED1, ADAR2, DRABA2, DRADA2 -ADARB1 and Liver Cancer
4
STARD13 13q13.1-q13.2 DLC2, GT650, ARHGAP37, LINC00464 -STARD13 and Liver Cancer
4
KIAA1524 3q13.13 p90, CIP2A -KIAA1524 and Hepatocellular Carcinoma
4
LDHA 11p15.1 LDHM, GSD11, PIG19, HEL-S-133P -LDHA and Liver Cancer
4
NOX4 11q14.3 KOX, KOX-1, RENOX -NOX4 and Liver Cancer
4
MT1G 16q13 MT1, MT1K -MT1G and Liver Cancer
4
CDC6 17q21.2 CDC18L, HsCDC6, MGORS5, HsCDC18 -CDC6 and Liver Cancer
4
HSPA1B 6p21.3 HSP70-2, HSP70.2, HSP70-1B -HSPA1B and Hepatocellular Carcinoma
4
TDGF1 3p21.31 CR, CRGF, CRIPTO -TDGF1 and Liver Cancer
4
MIR127 14q32.2 MIRN127, mir-127, miRNA127 -MIRN127 microRNA, human and Liver Cancer
4
LOXL2 8p21.3 LOR, LOR2, WS9-14 -LOXL2 and Liver Cancer
4
FZD7 2q33 FzE3 -FZD7 and Liver Cancer
4
CCNC 6q21 CycC -CCNC and Liver Cancer
4
CYP2B6 19q13.2 CPB6, EFVM, IIB1, P450, CYP2B, CYP2B7, CYP2B7P, CYPIIB6 -CYP2B6 and Hepatocellular Carcinoma
4
HPSE 4q21.23 HPA, HPA1, HPR1, HSE1, HPSE1 -HPSE and Liver Cancer
4
CD151 11p15.5 GP27, MER2, RAPH, SFA1, PETA-3, TSPAN24 -CD151 and Liver Cancer
4
YWHAZ 8q22.3 HEL4, YWHAD, KCIP-1, HEL-S-3, HEL-S-93, 14-3-3-zeta -YWHAZ and Liver Cancer
4
ATP7B 13q14.3 WD, PWD, WC1, WND -ATP7B and Liver Cancer
4
TP53INP1 8q22.1 SIP, Teap, p53DINP1, TP53DINP1, TP53INP1A, TP53INP1B -TP53INP1 and Liver Cancer
4
SLCO1B3 12p12.2 LST3, HBLRR, LST-2, OATP8, OATP-8, OATP1B3, SLC21A8, LST-3TM13 -SLCO1B3 and Liver Cancer
4
EREG 4q13.3 ER, Ep, EPR -EREG and Liver Cancer
4
UHRF1 19p13.3 Np95, hNP95, ICBP90, RNF106, TDRD22, hUHRF1, huNp95 -UHRF1 and Liver Cancer
4
GSTO1 10q25.1 P28, SPG-R, GSTO 1-1, GSTTLp28, HEL-S-21 -GSTO1 and Liver Cancer
4
IL23R 1p31.3 -IL23R and Liver Cancer
4
CCR6 6q27 BN-1, DCR2, DRY6, CCR-6, CD196, CKRL3, GPR29, CKR-L3, CMKBR6, GPRCY4, STRL22, CC-CKR-6, C-C CKR-6 -CCR6 and Liver Cancer
4
COPS5 8q13.1 CSN5, JAB1, SGN5, MOV-34 -COPS5 and Hepatocellular Carcinoma
4
PIM2 Xp11.23 -PIM2 and Liver Cancer
4
HLA-E 6p21.3 MHC, QA1, EA1.2, EA2.1, HLA-6.2 -HLA-E and Liver Cancer
4
PIK3CD 1p36.22 APDS, PI3K, IMD14, p110D, P110DELTA -PIK3CD and Liver Cancer
4
XRCC6 22q13.2 ML8, KU70, TLAA, CTC75, CTCBF, G22P1 -XRCC6 and Liver Cancer
4
MIR1301 2 MIRN1301, mir-1301, hsa-mir-1301 -MicroRNA miR-1301and Liver Cancer
4
MBL2 10q21.1 MBL, MBP, MBP1, MBPD, MBL2D, MBP-C, COLEC1, HSMBPC -MBL2 and Hepatocellular Carcinoma
4
RXRA 9q34.2 NR2B1 -RXRA and Liver Cancer
4
LGALS4 19q13.2 GAL4, L36LBP -LGALS4 and Liver Cancer
4
TRIO 5p15.2 tgat, MEBAS, MRD44, ARHGEF23 -TRIO and Hepatocellular Carcinoma
4
B2M 15q21.1 IMD43 -B2M and Liver Cancer
4
HOXA13 7p15.2 HOX1, HOX1J -HOXA13 and Liver Cancer
4
SLC9A1 1p36.11 APNH, NHE1, LIKNS, NHE-1, PPP1R143 -SLC9A1 and Liver Cancer
4
STAT4 2q32.2-q32.3 SLEB11 -STAT4 and Liver Cancer
4
GSTO2 10q25.1 GSTO 2-2, bA127L20.1 -GSTO2 and Liver Cancer
4
CDH17 8q22.1 HPT1, CDH16, HPT-1 -CDH17 and Liver Cancer
4
SOX1 13q34 -SOX1 and Liver Cancer
4
LEPR 1p31.3 OBR, OB-R, CD295, LEP-R, LEPRD -LEPR and Liver Cancer
4
STC1 8p21.2 STC -STC1 and Liver Cancer
4
EFEMP1 2p16 DHRD, DRAD, FBNL, MLVT, MTLV, S1-5, FBLN3, FIBL-3 -EFEMP1 and Liver Cancer
4
CEBPD 8q11.21 CELF, CRP3, C/EBP-delta, NF-IL6-beta -CEBPD and Hepatocellular Carcinoma
4
CD40 20q13.12 p50, Bp50, CDW40, TNFRSF5 -CD40 and Liver Cancer
4
S100A11 1q21.3 MLN70, S100C, HEL-S-43 -S100A11 and Liver Cancer
4
CCL19 9p13.3 ELC, CKb11, MIP3B, MIP-3b, SCYA19 -CCL19 and Liver Cancer
3
FMR1 Xq27.3 POF, FMRP, POF1, FRAXA -FMR1 and Liver Cancer
3
HSP90AA1 14q32.31 EL52, HSPN, LAP2, HSP86, HSPC1, HSPCA, Hsp89, Hsp90, LAP-2, HSP89A, HSP90A, HSP90N, Hsp103, HSPCAL1, HSPCAL4, HEL-S-65p -HSP90AA1 and Liver Cancer
3
MAPK3 16p11.2 ERK1, ERT2, ERK-1, PRKM3, P44ERK1, P44MAPK, HS44KDAP, HUMKER1A, p44-ERK1, p44-MAPK -MAPK3 and Liver Cancer
3
RALBP1 18p11.22 RIP1, RLIP1, RLIP76 -RALBP1 and Liver Cancer
3
MAGEB2 Xp21.2 DAM6, CT3.2, MAGE-XP-2 -MAGEB2 and Liver Cancer
3
ZNF331 19q13.42 RITA, ZNF361, ZNF463 -ZNF331 and Liver Cancer
3
CSTB 21q22.3 PME, ULD, CST6, EPM1, STFB, CPI-B, EPM1A -CSTB and Liver Cancer
3
HHIP 4q31.21 HIP -HHIP and Liver Cancer
3
DEC1 9q33.1 CTS9 -DEC1 and Liver Cancer
3
MEF2C 5q14.3 DEL5q14.3, C5DELq14.3 -MEF2C and Liver Cancer
3
BNIP3L 8p21.2 NIX, BNIP3a -BNIP3L and Hepatocellular Carcinoma
3
MIR34A 1p36.22 mir-34, MIRN34A, mir-34a, miRNA34A -MIR34A and Liver Cancer
3
TNFRSF6B 20q13.33 M68, TR6, DCR3, M68E, DJ583P15.1.1 -TNFRSF6B expression in Hepatocellular Carcinoma (HCC)
3
CSMD1 8p23.2 PPP1R24 -CSMD1 and Liver Cancer
3
SMAD6 15q22.31 AOVD2, MADH6, MADH7, HsT17432 -SMAD6 and Liver Cancer
3
IFT88 13q12.11 DAF19, TG737, TTC10, hTg737, D13S1056E -IFT88 and Hepatocellular Carcinoma
3
EPHA1 7q34-q35 EPH, EPHT, EPHT1 -EPHA1 and Liver Cancer
3
RAD23B 9q31.2 P58, HR23B, HHR23B -RAD23B and Hepatocellular Carcinoma
3
SPRY1 4q28.1 hSPRY1 -SPRY1 and Hepatocellular Carcinoma
3
PTPRT 20q12-q13.11 RPTPrho -PTPRT and Hepatocellular Carcinoma
3
OCLN 5q13.2 BLCPMG, PPP1R115 -OCLN and Liver Cancer
3
DLEC1 3p22.2 F56, DLC1, DLC-1, CFAP81 -DLEC1 and Liver Cancer
3
DMPK 19q13.32 DM, DM1, DMK, MDPK, DM1PK, MT-PK -DMPK and Liver Cancer
3
IRF9 14q12 p48, IRF-9, ISGF3, ISGF3G -IRF9 and Hepatocellular Carcinoma
3
TNFRSF10C 8p21.3 LIT, DCR1, TRID, CD263, TRAILR3, TRAIL-R3, DCR1-TNFR -TNFRSF10C and Liver Cancer
3
CD276 15q24.1 B7H3, B7-H3, B7RP-2, 4Ig-B7-H3 -CD276 and Liver Cancer
3
ANXA5 4q27 PP4, ANX5, ENX2, RPRGL3, HEL-S-7 -ANXA5 and Liver Cancer
3
PTMS 12p13 ParaT -PTMS and Liver Cancer
3
TBX3 12q24.21 UMS, XHL, TBX3-ISO -TBX3 and Liver Cancer
3
RAC2 22q13.1 Gx, EN-7, HSPC022, p21-Rac2 -RAC2 and Liver Cancer
3
EBAG9 8q23.2 EB9, PDAF -EBAG9 and Liver Cancer
3
FEN1 11q12.2 MF1, RAD2, FEN-1 -FEN1 and Liver Cancer
3
UCP2 11q13.4 UCPH, BMIQ4, SLC25A8 -UCP2 and Liver Cancer
3
CXCL14 5q31.1 KEC, KS1, BMAC, BRAK, NJAC, MIP2G, MIP-2g, SCYB14 -CXCL14 and Liver Cancer
3
SERPINC1 1q25.1 AT3, AT3D, ATIII, THPH7, ATIII-R2, ATIII-T1, ATIII-T2 -SERPINC1 and Liver Cancer
3
TRIM24 7q33-q34 PTC6, TF1A, TIF1, RNF82, TIF1A, hTIF1, TIF1ALPHA -TRIM24 and Liver Cancer
3
CCR1 3p21 CKR1, CD191, CKR-1, HM145, CMKBR1, MIP1aR, SCYAR1 -CCR1 and Hepatocellular Carcinoma
3
ING2 4q35.1 ING1L, p33ING2 -ING2 and Liver Cancer
3
IL24 1q32.1 C49A, FISP, MDA7, MOB5, ST16, IL10B -IL24 and Liver Cancer
3
VCAM1 1p21.2 CD106, INCAM-100 -VCAM1 and Liver Cancer
3
PPIA 7p13 CYPA, CYPH, HEL-S-69p -PPIA and Liver Cancer
3
AKR1C2 10p15.1 DD, DD2, TDD, BABP, DD-2, DDH2, HBAB, HAKRD, MCDR2, SRXY8, DD/BABP, AKR1C-pseudo -AKR1C2 and Liver Cancer
3
S100A10 1q21.3 42C, P11, p10, GP11, ANX2L, CAL1L, CLP11, Ca[1], ANX2LG -S100A10 and Liver Cancer
3
CHGA 14q32.12 CGA -CHGA and Liver Cancer
3
BAGE 21p11.1 BAGE1, CT2.1 -BAGE and Liver Cancer
3
ROCK2 2p24 ROCK-II -ROCK2 and Liver Cancer
3
AGTR2 Xq23 AT2, ATGR2, MRX88 -AGTR2 and Liver Cancer
3
MERTK 2q14.1 MER, RP38, c-Eyk, c-mer, Tyro12 -MERTK and Liver Cancer
2
EPHA5 4q13.1-q13.2 EK7, CEK7, EHK1, HEK7, EHK-1, TYRO4 -EPHA5 and Liver Cancer
2
PPP1R3A 7q31.1 GM, PP1G, PPP1R3 -PPP1R3A and Liver Cancer
2
GMNN 6p22.3 Gem -GMNN and Liver Cancer
2
HTRA2 2p12 OMI, PARK13, PRSS25 -HTRA2 and Liver Cancer
2
SLC22A18 11p15.4 HET, ITM, BWR1A, IMPT1, TSSC5, ORCTL2, BWSCR1A, SLC22A1L, p45-BWR1A -SLC22A18 and Liver Cancer
2
ZFP36 19q13.2 TTP, G0S24, GOS24, TIS11, NUP475, zfp-36, RNF162A -ZFP36 and Liver Cancer
2
LIPA 10q23.31 LAL, CESD -LIPA and Liver Cancer
2
CSE1L 20q13.13 CAS, CSE1, XPO2 -CSE1L and Liver Cancer
2
CA12 15q22.2 CAXII, CA-XII, T18816, HsT18816 -CA12 and Liver Cancer
2
PRSS1 7q34 TRP1, TRY1, TRY4, TRYP1 -PRSS1 and Liver Cancer
2
FABP5 8q21.13 EFABP, KFABP, E-FABP, PAFABP, PA-FABP -FABP5 and Liver Cancer
2
RASAL1 12q24.13 RASAL -RASAL1 and Liver Cancer
2
ELF4 Xq26.1 MEF, ELFR -ELF4 and Liver Cancer
2
LTBR 12p13 CD18, TNFCR, TNFR3, D12S370, TNFR-RP, TNFRSF3, TNFR2-RP, LT-BETA-R, TNF-R-III -LTBR and Liver Cancer
2
MIR1297 13q14.3 MIRN1297, mir-1297, hsa-mir-1297 -MIRN1297 microRNA, human and Liver Cancer
2
MUC7 4q13.3 MG2 -MUC7 and Hepatocellular Carcinoma
2
PDCD5 19q13.11 TFAR19 -PDCD5 and Liver Cancer
2
MIR124-1 8p23.1 MIR124A, MIR124A1, MIRN124-1, MIRN124A1, mir-124-1 -microRNA 124-1 and Liver Cancer
2
SNRPE 1q32.1 SME, Sm-E, HYPT11, snRNP-E -SNRPE and Liver Cancer
2
SRSF3 6p21.31-p21.2 SFRS3, SRp20 -SRSF3 and Liver Cancer
2
KRT18 12q13.13 K18, CK-18, CYK18 -KRT18 and Liver Cancer
2
DDIT4 10q22.1 Dig2, REDD1, REDD-1 -DDIT4 and Liver Cancer
2
ANXA7 10q22.2 SNX, ANX7, SYNEXIN -ANXA7 and Liver Cancer
2
SAT2 17p13.1 SSAT2 -SAT2 and Liver Cancer
2
FTL 19q13.33 LFTD, NBIA3 -FTL and Liver Cancer
2
CXCL16 17p13.2 SRPSOX, CXCLG16, SR-PSOX -CXCL16 and Liver Cancer
2
THRAP3 1p34.3 BCLAF2, TRAP150 -THRAP3 and Liver Cancer
2
ITGA6 2q31.1 CD49f, VLA-6, ITGA6B -ITGA6 and Liver Cancer
2
YWHAE 17p13.3 MDS, HEL2, MDCR, KCIP-1, 14-3-3E -YWHAE and Liver Cancer
2
DNAJB4 1p31.1 DjB4, HLJ1, DNAJW -DNAJB4 and Liver Cancer
2
GJB2 13q12.11 HID, KID, PPK, CX26, DFNA3, DFNB1, NSRD1, DFNA3A, DFNB1A -GJB2 and Hepatocellular Carcinoma
2
IGF2-AS 11p15.5 PEG8, IGF2AS, IGF2-AS1 -IGF2-AS and Liver Cancer
2
KRT8 12q13 K8, KO, CK8, CK-8, CYK8, K2C8, CARD2 -KRT8 and Liver Cancer
2
THBS2 6q27 TSP2 -THBS2 and Hepatocellular Carcinoma
2
CCR3 3p21.3 CKR3, CD193, CMKBR3, CC-CKR-3 -CCR3 and Liver Cancer
2
ING3 7q31.31 Eaf4, ING2, MEAF4, p47ING3 -ING3 and Liver Cancer
2
SOX6 11p15.2 SOXD, HSSOX6 -SOX6 and Liver Cancer
2
MRTFA 22q13.1-q13.2 MAL, MKL, BSAC, MKL1, MRTF-A -MKL1 and Liver Cancer
2
MIR125A 19q13.41 MIRN125A, mir-125a, miRNA125A -MIR125A and Liver Cancer
1
NOV 8q24.12 CCN3, NOVh, IBP-9, IGFBP9, IGFBP-9 -NOV and Liver Cancer
1
MIR1271 5q35.2 MIRN1271, hsa-mir-1271 -MicroRNA miR-1271 and Liver Cancer
1
KTN1 14q22.3 CG1, KNT, MU-RMS-40.19 -KTN1 and Liver Cancer
1
SLC9A3R1 17q25.1 EBP50, NHERF, NHERF1, NHERF-1, NPHLOP2 -SLC9A3R1 and Hepatocellular Carcinoma
1
CCKBR 11p15.4 GASR, CCK-B, CCK2R -CCKBR and Liver Cancer
1
ERC1 12p13.33 ELKS, Cast2, ERC-1, RAB6IP2 -ERC1 and Liver Cancer
1
EPB41 1p35.3 HE, EL1, 4.1R -EPB41 and Liver Cancer
1
GOLGA5 14q32.12 RFG5, GOLIM5, ret-II -GOLGA5 and Liver Cancer
1
BRINP1 9q33.1 DBC1, FAM5A, DBCCR1 -BRINP1 and Liver Cancer
1
IFNA17 9p21.3 IFNA, INFA, LEIF2C1, IFN-alphaI -IFNA17 and Hepatocellular Carcinoma
ANXA8 10q11.22 ANX8, CH17-360D5.2 -ANXA8 and Liver Cancer
SELENOP 5p12 SeP, SELP, SEPP, SEPP1 -SEPP1 and Hepatocellular Carcinoma
PECAM1 17q23.3 CD31, PECA1, GPIIA', PECAM-1, endoCAM, CD31/EndoCAM -PECAM1 and Liver Cancer
IFNA2 9p21.3 IFNA, INFA2, IFNA2B, IFN-alphaA -IFNA2 and Hepatocellular Carcinoma
IFNA7 9p21.3 IFNA-J, IFN-alphaJ -IFNA7 and Hepatocellular Carcinoma
MYBL2 20q13.12 BMYB, B-MYB -MYBL2 and HCC

Note: list is not exhaustive. Number of papers are based on searches of PubMed (click on topic title for arbitrary criteria used).

Latest Publications

Amisaki M, Yagyu T, Uchinaka EI, et al.
Prognostic Value of DEPDC1 Expression in Tumor and Non-tumor Tissue of Patients With Hepatocellular Carcinoma.
Anticancer Res. 2019; 39(8):4423-4430 [PubMed] Related Publications
BACKGROUND/AIM: To evaluate the impact of DEPDC1 expression on patient prognosis after hepatic resection for hepatocellular carcinoma (HCC).
PATIENTS AND METHODS: We reviewed data from 75 patients who underwent hepatic resection for HCC between 2004 and 2013. Recurrence at 2 years following resection, which mainly included metastatic recurrence, was defined as late recurrence.
RESULTS: DEPDC1 was up-regulated in HCC tissue and in non-tumor tissue of patients with HCC compared to normal liver (p<0.01 and p<0.01, respectively). High expression of DEPDC1 was associated with poor overall, disease-specific, and disease-free survival (p=0.02, p<0.01, and p<0.01, respectively). High DEPDC1 expression was an independent predictor of death and recurrence (p=0.03 and p<0.01, respectively). High expression of DEPDC1 in non-tumor liver was an independent risk factor for late recurrence (p=0.04).
CONCLUSION: High expression of DEPDC1 in tumor tissue appears to be associated with tumor progression and poor prognosis.

Yang J, Liu J, Chen Y, et al.
Association of CTLA-4 tagging polymorphisms and haplotypes with hepatocellular carcinoma risk: A case-control study.
Medicine (Baltimore). 2019; 98(29):e16266 [PubMed] Related Publications
It has been proposed that cytotoxic T-lymphocyte antigen 4 (CTLA-4) may attenuate the T-cell activation threshold, thereby decreasing the antitumor response and conferring susceptibility to hepatocellular carcinoma (HCC).In the present study, we selected CTLA-4 tagging single nucleotide polymorphisms (SNPs) and explored the relationship between these polymorphisms and susceptibility to HCC. A hospital-based case-control study, comprising 584 cases with HCC and 923 controls, was performed in an eastern Chinese Han population. CTLA-4 SNPs were genotyped using a custom-by-design 48-Plex SNPscan Kit.We found that the CTLA-4 rs3087243 G>A polymorphism might be associated with increased risk of HCC (GA vs GG: adjusted odds ratio [OR], 1.38; 95% confidence interval [CI], 1.04-1.85; P = .028 and AA/GA vs GG: adjusted OR, 1.43; 95% CI, 1.08-1.89; P = .012). After using Bonferroni correction, this association remained (P = .012 for the AA/GA vs GG genetic model). In addition, the power value was 0.904 in the AA/GA versus GG genetic model. Haplotype analysis showed that CTLA4 Crs16840252Ars231775Ars3087243Trs733618, Crs16840252Grs231775Ars3087243Trs733618, and other haplotypes might increase the risk of HCC risk (P = .018, <.001, and .017, respectively). However, we found that CTLA4 Trs16840252A rs231775Grs3087243Trs733618 decreased the risk of HCC (P = .020).Our results suggest that the CTLA-4 rs3087243 G>A polymorphism increases susceptibility to HCC in an eastern Chinese Han population. CTLA-4 haplotypes may influence the development of HCC. In the future, a population-based fine-mapping study with functional assessment should be performed to further determine these potential correlations.

Liu L, Qi X, Gui Y, et al.
Overexpression of circ_0021093 circular RNA forecasts an unfavorable prognosis and facilitates cell progression by targeting the miR-766-3p/MTA3 pathway in hepatocellular carcinoma.
Gene. 2019; 714:143992 [PubMed] Related Publications
Increasing studies have demonstrated the important roles of circular RNAs (circRNAs) in human malignancies. Nevertheless, the molecular mechanisms and functions of circRNAs in hepatocellular carcinoma (HCC) are still not fully understood. In the present study, we evaluated circ_0021093 expression in 82 pairs of HCC tissues and 5 cell lines by qRT-PCR. The clinical implications of circ_0021093 were evaluated. In addition, the viability, apoptosis, migration and invasion capacities of different HCC cells were evaluated by gain-/loss-of-function experiments. Target prediction and dual-luciferase reporter experiments were performed to identify the molecular mechanisms of circ_0021093. Upregulation of circ_0021093 was found in HCC tumor samples and cells. Additionally, upregulated circ_0021093 was related to adverse clinical characteristics and an unfavorable prognosis. Furthermore, downregulated circ_0021093 attenuated cell growth, migration and invasion but increased cell apoptosis. By contrast, ectopically expressed circ_0021093 enhanced the abovementioned malignant biological behaviors. For mechanism exploration, circ_0021093 sponges of miR-766-3p were used in HCC cells. In addition, we found that metastasis-associated protein 3 (MTA3) was a direct target of miR-766-3p and that the oncogenic function of circ_0021093 was partly dependent on the miR-766-3p/MTA3 axis according to rescue assays. In conclusion, the circ_0021093/miR-766-3p/MTA3 regulatory axis may be an effective therapeutic target for HCC.

Huang D, Wei Y, Zhu J, Wang F
Long non-coding RNA SNHG1 functions as a competitive endogenous RNA to regulate PDCD4 expression by sponging miR-195-5p in hepatocellular carcinoma.
Gene. 2019; 714:143994 [PubMed] Related Publications
Long non-coding RNA (lncRNA) potentially regulates tumorigenesis. LncRNA small nucleolar RNA host gene 1 (SNHG1) expression remains high in hepatocellular carcinoma cells; however, its biological mechanism in hepatocellular carcinoma remains unknown. In this study, SNHG1 expression in hepatocellular carcinoma cells was detected by qRT-PCR. Proliferative and migratory potentials of hepatocellular carcinoma cells were determined by CCK-8 and Transwell assay, respectively. Then, the nude mice model of xenograft was employed to verify the effect of SNHG1 on tumor formation in vivo. We identified the potential target of SNHG1 through bioinformatics and dual-luciferase reporter gene. Furthermore, Western blot and RIP assay was used for clarifying their interaction and functions in regulating the development of hepatocellular carcinoma. Our results indicated a high expression of SNHG1 in hepatocellular carcinoma cells. Downregulation of SNHG1 inhibited proliferative and migratory potentials of hepatocellular carcinoma cells in vitro and in vivo. Moreover, the expression of programmed cell death 4 (PDCD4) was positively regulated by SNHG1 through competing with miR-195-5p. These results indicated that SNHG1 participated in the development of hepatocellular carcinoma as a ceRNA to competitively bind to miR-195-5p and thus mediate PDCD4 expression.

Cao L, Hong J, Wang Y, et al.
A primary splenic angiosarcoma hepatic metastasis after splenectomy and its genomic alteration profile.
Medicine (Baltimore). 2019; 98(28):e16245 [PubMed] Free Access to Full Article Related Publications
RATIONALE: Primary splenic angiosarcoma (PSA) is a rare mesenchymal malignancy of the splenic vascular origin often with a dismal prognosis. Genomic profile may provide evidence for the solution of therapy.
PATIENT CONCERNS: We reported a case of a 51-year-old woman with splenectomy 4 years ago and the postoperative histopathology diagnosis revealed "splenic hemangioma" with spontaneous rupture. Two years after the operation, the patient's rechecked abdominal computed tomography (CT) showed multiple hepatic occupations.
DIAGNOSES: Pathological test suggested PSA hepatic metastasis.
INTERVENTIONS: The patient was treated with trans-catheter arterial chemoembolization (TACE) and a pathological diagnosis of PSA was highly suspected in the hepatic biopsy. Four somatic alterations, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA), Fos proto-oncogene, AP-1 transcription factor subunit (FOS), MCL1 apoptosis regulator (MCL1), and phosphoinositide-3-kinase regulatory subunit 1 (PIK3R1) were detected in the tumor tissue using a Next generation sequencing (NGS) technology. The results prompted that the patient may get clinical benefit from using some agents for targeted therapy, Everolimus, Temsirolimus, or Copanlisib.
OUTCOMES: The patient refused targeted therapy. As a result, the patient passed away within 51 months after splenectomy.
LESSONS: PSA is an aggressive disease that often presented with a high propensity for metastasis and rupture hemorrhage. Some of these mutations were first discovered in PSA and these findings added new contents to the genomic mutation profile of PSA.

Song T, Liu JY, Yang JJ
NKAP plays an oncogenic function partly through AKT signaling pathway in hepatocellular carcinoma.
Neoplasma. 2019; 2019 [PubMed] Related Publications
NF-kB activating protein (NKAP) is a highly conserved protein involved in transcriptional repression, immune cell development, maturation, T cell acquisition of functional competency and maintenance of hematopoiesis. Here we first explore the function of NKAP in hepatocellular carcinoma (HCC). We found that NKAP was highly expressed in HCC tissues and associated with a poor patient survival. CCK8 assay showed that NKAP knockdown significantly decreased cell viability of HuH7 and Hep3B HCC cell lines. Cell invasion, tested by transwell assays, was significantly inhibited by NKAP knockdown in HuH7 and Hep3B cells (P<0.05). Percentage of cell apoptosis was significantly increased by NKAP knockdown in HuH7 cells (6.5% to 12.5%) and in Hep3B cells (8.3% to 27.3%). Furthermore, western blot results indicated that NKAP silence upregulated the expression of pro-apoptotic proteins Bax and Caspase3-P17 while downregulated anti-apoptotic protein Bcl2. Finaly, AKT signaling pathway was evaluated to reveal the underlying mechanism of NKAP in HCC cells. It was suggested that NKAP knockdown decreased the phosphorylation level of AKT and the expression of its downstream members p70S6K and Cyclin D1. Furthermore, we demonstrated that NKAP knockdown also played an oncogenic role in human gastric cancer AGS and MKN45 cells. In conclusion, for the first time our study reveals that NKAP promotes the proliferation and invasion in HCC cell lines at least partly through AKT signaling pathway.

Yari K, Jalilvand A
Comment on: 'A 40-bp insertion/deletion polymorphism in the constitutive promoter of MDM2 confers risk for hepatocellular carcinoma in a Chinese population'.
Gene. 2019; 712:143965 [PubMed] Related Publications
Recently, we read the published article in GENE. Dong et al. presented the evaluation of the MDM2 40-bp insertion/deletion status in Hepatocellular carcinoma patients (Dong et al., 2012). The authors stated that the insertion allele showed a 521-bp band and the deletion allele showed a 481-bp band on agarose gel electrophoresis. While it seems that these reported sizes for insertion and deletion alleles of MDM2 are incorrect. Our analysis using the primers indicated that the length of insertion and deletion fragments will be 481 and 441 bps, respectively. Actually, 40-bp is added to the fragment length instead of reducing the 40-bp. In the 'UCSC In-Silico PCR' tool, the length of the amplified fragment using mentioned primers is 481-bp including the sequence of 40-bp insertion allele (5'-(A)

Zhang H, Luo C, Zhang G
LncRNA
DNA Cell Biol. 2019; 38(8):857-864 [PubMed] Related Publications
Hepatocellular carcinoma (HCC) has been reported to be one of the major tumors in the world. There is a study indicating that MCM3AP-AS1 is an oncogenic factor in HCC; however, the mechanism by which MCM3AP-AS1 regulates HCC remains not fully understood. Reverse Transcription-quantitative PCR and Western blot approaches were used to detect mRNA and protein levels of various genes. To examine invasion of HCC cells and lymphatic vessel formation of human dermal lymphatic endothelial cells (HDLECs), we employed transwell invasion assay and lymphatic vessel assay. Bioinformatic analysis and luciferase reporter assay were used to establish direct interactions between MCM3AP-AS1 and miR-455. Besides, The Cancer Genome Atlas analyses of HCCs were performed to determine the association of MCM3AP-AS1 and epidermal growth factor receptor (EGFR) with overall survival. MCM3AP-AS1 knockdown impaired invasion of HCC cells and lymphatic vessel formation of HDLECs. MCM3AP-AS1 directly interacted with miR-455. Furthermore, miR-455 inhibitor-transfected HepG2 cells enhanced the invasion and lymphatic vessel formation abilities. The rescue experiments indicated that EGFR was critical for MCM3AP-AS1- and miR-455-regulated invasion and lymphatic vessel formation. More interestingly, autophagy-related genes (Beclin1, LC3 II/I, and ATG7) were abnormally regulated in miR-455 mimic or inhibitor HepG2 cells. miR-455 mimic inhibited cell invasion and lymphatic vessel formation, which was evidently abrogated by ATG7 overexpression. Finally, we analyzed The Cancer Genome Atlas data sets to test the upregulated expression levels of MCM3AP-AS1 and EGFR. In addition, the results showed that low levels of both genes facilitate survival of HCC patients. In this study, we reveal a novel mechanism underlying MCM3AP-AS1-induced HCC metastasis by regulating miR-455. The conclusions provide more insights into understanding mechanism underlying HCC and help development of therapeutical approaches for treating HCC.

Okamura K, Nakabayashi K, Kawai T, et al.
DNA methylation changes involved in the tumor increase in F2 males born to gestationally arsenite-exposed F1 male mice.
Cancer Sci. 2019; 110(8):2629-2642 [PubMed] Free Access to Full Article Related Publications
Multigenerational adverse effects from the environment such as nutrition and chemicals are among important concerns in environmental health issues. Previously, we have found that arsenite exposure of only F0 females during their pregnancy increases hepatic tumors in the F2 males in C3H mice. In the current study, we investigated the association of DNA methylation with the hepatic tumor increase in the F2 males of the arsenite group. Reduced-representation bisulfite sequencing analysis newly identified that DNA methylation levels of regions around the transcriptional start sites of Tmem54 and Cd74 were decreased and the expression of these genes were significantly increased in the hepatic tumors of F2 males of the arsenite group. The associations between DNA methylation in these regions and gene expression changes were confirmed by treatment of murine hepatoma cell lines and hepatic stellate cell line with 5-aza-2'-deoxycytidine. Overexpression of Cd74 in Hepa1c1c7 cells increased Trib3 expression and suppressed the expression of tumor suppressor genes Id3 and Atoh8. Human database analysis using the Cancer Genome Atlas indicated that TMEM54, CD74, and TRIB3 were significantly increased and that ATOH8 was decreased in hepatocellular carcinoma. The data also showed that high expression of TMEM54 and TRIB3 and low expression of ATOH8 were associated with poor survival. These results suggested that an increase in Tmem54 and Cd74 expression via DNA methylation reduction was involved in the tumor increase in the F2 male offspring by gestational arsenite exposure of F0 females. This study also suggested that genes downstream of Cd74 were involved in tumorigenesis.

Chen TW, Yin FF, Yuan YM, et al.
CHML promotes liver cancer metastasis by facilitating Rab14 recycle.
Nat Commun. 2019; 10(1):2510 [PubMed] Free Access to Full Article Related Publications
Metastasis-associated recurrence is the major cause of poor prognosis in hepatocellular carcinoma (HCC), however, the underlying mechanisms remain largely elusive. In this study, we report that expression of choroideremia-like (CHML) is increased in HCC, associated with poor survival, early recurrence and more satellite nodules in HCC patients. CHML promotes migration, invasion and metastasis of HCC cells, in a Rab14-dependent manner. Mechanism study reveals that CHML facilitates constant recycling of Rab14 by escorting Rab14 to the membrane. Furthermore, we identify several metastasis regulators as cargoes carried by Rab14-positive vesicles, including Mucin13 and CD44, which may contribute to metastasis-promoting effects of CHML. Altogether, our data establish CHML as a potential promoter of HCC metastasis, and the CHML-Rab14 axis may be a promising therapeutic target for HCC.

Zhao S, Li J, Zhang G, et al.
Exosomal miR-451a Functions as a Tumor Suppressor in Hepatocellular Carcinoma by Targeting LPIN1.
Cell Physiol Biochem. 2019; 53(1):19-35 [PubMed] Related Publications
BACKGROUND/AIMS: Emerging evidence suggests that exosomal microRNAs (miRNAs) mediate hepatoma progression through the post-translational regulation of their targets. However, characteristically-expressed miRNAs and their functions in the tumor and tumor-associated angiogenesis remain poorly understood.
METHODS: miRNA sequencing (HiSeq 2500 SE50) was performed to identify miRNA species that are involved in the hepatocellular carcinoma (HCC) pathogenesis. We identified miR-451a downregulation according to its expression and TCGA analysis. miR-451a was found to be mainly involved in cell viability, apoptosis, cell cycle and migration both in HCC and endothelial cell lines. LPIN1 was predicted to be a target of this miRNA based on TargetScan, GSEA analysis, and the Uniprot database. We performed real time PCR and dual luciferase assays to confirm these results.
RESULTS: We identified that miR-451a is significantly downregulated in serum-derived exosomes from HCC patients, as compared to expression in those from normal individuals. We further confirmed that overexpression of miR-451a functions in HCC and endothelia cells in vitro and in vivo. Exosomal miR-451a, as a tumor suppressor, was found to induce apoptosis both in HCC cell lines and human umbilical vein endothelial cells (HUVECs). In addition, miR-451a suppressed HUVEC migration, tube formation, and vascular permeability. Importantly, we demonstrated that LPIN1 is a critical target of miR-451a, and promotes apoptosis in both HCC and endothelial cells.
CONCLUSION: Our study provides the novel finding that exosomal miR-451a targets LPIN1 to inhibit hepatocellular tumorigenesis by regulating tumor cell apoptosis and angiogenesis. These results have clinical implications regarding the deregulation of miRNAs in HCC.

Wendling-Keim D, Vokuhl C, Walz C, et al.
Activation of Hedgehog Signaling in Aggressive Hepatic Hemangioma in Newborns and Infants.
Anticancer Res. 2019; 39(5):2351-2360 [PubMed] Related Publications
BACKGROUND/AIM: Hepatic hemangiomas (HH) can show an aggressive course with significant complications. Prognostic markers that identify an aggressive course are entirely absent. Since we have showed that Hedgehog signaling is overexpressed in aggressive hemangiomas of the skin. Here, we hypothesize that it is also altered in aggressive HH.
MATERIALS AND METHODS: Immunohistological staining for GLUT1 and quantitative PCR was performed in seven specimens with aggressive HH. For comparison, we included specimens of kaposiform hemangioendothelioma (KHE), skin hemangioma and normal liver tissue.
RESULTS: Overexpression of the Hedgehog signaling components SHH and GLI2 and its target gene FOXA2 in HH were similar to those found in aggressive skin hemangioma and KHE, their expression being significantly higher than in mild skin hemangioma. High expression levels of SHH and FOXA2 positively correlated with HH, but not with normal liver tissue.
CONCLUSION: Hedgehog signaling is up-regulated in aggressive HH. This finding may lead to a biomarker allowing early intervention.

Hu Y, Liu Q, Zhou XF, et al.
[Screening of optimal siRNA interference sequence of CIT gene and its inhibition expression in hepatoma SK-Hep-1].
Zhonghua Gan Zang Bing Za Zhi. 2019; 27(4):281-285 [PubMed] Related Publications

Li B, Liu D, Yang P, et al.
miR-613 inhibits liver cancer stem cell expansion by regulating SOX9 pathway.
Gene. 2019; 707:78-85 [PubMed] Related Publications
Liver cancer stem cells (CSCs) contribute to tumorigenesis, progression, drug resistance and recurrence of hepatocellular carcinoma (HCC). However, the underlying mechanism for the propagation of liver CSCs remains unclear. Herein, we observed miR-613 expression was downregulated in both chemoresistant and recurrent HCC patients. A remarkable decrease in miR-613 was detected in CD24 or OV6-positive liver CSCs and CSC-enriched hepatoma spheres. Down-regulation of miR-613 facilitated liver CSCs expansion by promoting the dedifferentiation of hepatoma cells and enhancing the self-renewal of liver CSCs. Mechanistically, bioinformatic and luciferase reporter analysis identified SOX9 as a direct target of miR-613. Overexpression of miR-613 inhibited the expression of SOX9 in HCC cells. Special SOX9 siRNA abolished the discrepancy in liver CSCs proportion and the self-renewal capacity between miR-613 overexpression hepatoma cells and control cells, which further confirmed that SOX9 was required in miR-613-inhibited liver CSCs expansion. Furthermore, hepatoma cells with miR-613 overexpression performed more sensitivity to cisplatin or sorafenib treatment. Conclusion: miR-613 could inhibit HCC cell dedifferentiation and liver CSCs expansion by targeting SOX9 signaling and may prove to be a novel therapeutic target for HCC patients.

Lin X, Chai G, Wu Y, et al.
RNA m
Nat Commun. 2019; 10(1):2065 [PubMed] Free Access to Full Article Related Publications
N6-Methyladenosine (m

Cao H, Chu X, Wang Z, et al.
High FOXK1 expression correlates with poor outcomes in hepatocellular carcinoma and regulates stemness of hepatocellular carcinoma cells.
Life Sci. 2019; 228:128-134 [PubMed] Related Publications
AIMS: Forkhead box (FOX) proteins constitute a huge family of transcriptional regulators, which are involved in a wide range of cancers. FOXK1 is a little studied member of FOXK subfamily. This study aimed to investigate the potential prognostic value of FOXK1 in human hepatocellular carcinoma (HCC) and explore potential underlying mechanisms.
MAIN METHODS: We performed bioinformatic analyses to evaluate the prognostic value of FOXK1 expression in human HCC and to reveal the underlying mechanism by which FOXK1 regulates HCC. RT-PCR, FACS analysis and sphere formation assay were carried out to investigate the role of FOXK1 in regulating liver cancer stem cells.
KEY FINDINGS: Our results demonstrated that FOXK1 was overexpressed in human HCC and positively correlated with cancer progression. DNA hypomethylation and gene copy number variation contributed to the overexpression of FOXK1. Importantly, high FOXK1 expression was associated with both low overall survival probability (OS) and low relapse free survival probability (RFS) of HCC patients. Intriguingly, we found that high FOXK1 expression was correlated with activation of stem cell-regulating pathways in human HCC. Knockdown of FOXK1 resulted in downregulation of the cancer stem cell marker EpCAM and ALDH1 and decreased sphere-forming ability of hepatocellular carcinoma cells.
SIGNIFICANCE: Overall, our study identified FOXK1 as a new biomarker for prognosis of HCC patients and revealed its role in regulating stemness of hepatocellular carcinoma cells.

Guo D, Li Y, Chen Y, et al.
DANCR promotes HCC progression and regulates EMT by sponging miR-27a-3p via ROCK1/LIMK1/COFILIN1 pathway.
Cell Prolif. 2019; 52(4):e12628 [PubMed] Related Publications
OBJECTIVES: This research aims to verify that the long non-coding RNA differentiation antagonizing nonprotein coding RNA (LncRNA DANCR) could modulate the proliferation and metastasis of hepatocellular carcinoma (HCC), and it thus may work as a novel biomarker to render new orientation for early diagnosis and clinical therapy of HCC.
MATERIALS AND METHODS: Firstly, qRT-PCR was used to detect the expression of genes including LncRNA DANCR and miR-27a-3p. Next, MTT assay, Ethynyldeoxyuridine (EdU) analysis and clone formation assay were used for investigating cell growth and proliferation. Meanwhile, transwell assay and wound healing assay were applied to evaluate the capacity of cell metastasis and motility, respectively. In addition, bioinformatic analysis and dual-luciferase reporter assay were applied to analyse molecular interaction. Next, we conducted immunofluorescence and Western blot for mechanic investigation. Last but not the least, xenograft tumours in nude mice were built by subcutaneously injecting Hep3B cells stably transfected with sh-NC and sh-DANCR to detect proliferation and SMMC-7721 cells stably transfected with sh-NC and sh-DANCR to investigate metastasis.
RESULTS: The results of qRT-PCR and bioinformatic analysis revealed the high expression of DANCR in HCC. DANCR accelerated proliferation and metastasis of HCC cells and the knockdown of DANCR had the opposite effect. Meanwhile, xenograft tumours in sh-DANCR group grow slower and have smaller volumes compared with negative control group. Next, the antineoplastic effect of miR-27a-3p on cell growth and motility of HCC was confirmed. In addition, we clarified that DANCR acted as a ceRNA to decoy miR-27a-3p via mediating ROCK1/LIMK1/COFILIN1 pathway. In the end, we validated that DANCR/miR-27a-3p axis regulates EMT progression by cell immunofluorescence and Western blot.
CONCLUSIONS: In a word, DANCR promotes HCC development and induces EMT by decoying miR-27a-3p to regulate ROCK1/LIMK1/COFILIN1 pathway.

Ahmed MY, Salah MM, Kassim SK, et al.
Evaluation of the diagnostic and therapeutic roles of non-coding RNA and cell proliferation related gene association in hepatocellular carcinoma.
Gene. 2019; 706:97-105 [PubMed] Related Publications
Micro RNA-34a-5p (miR-34a-5p) is an important molecule that can act as a modulator of tumor growth. It controls expression of a plenty of proteins controlling cell cycle, differentiation and apoptosis and opposing processes that favor viability of cancer cells, their metastasis and resistance to chemotherapy. Bioinformatics analysis indicated that minichromosome maintenance protein 2 (MCM2) is a target gene of miR-34a-p. In this study, RT-qPCR was employed to detect the expression of miR-34a-5p and MCM2 in 10 hepatocellular carcinoma (HCC) tissues. The functional role of miR-34a-5p in HCC was investigated and the interaction between miR-34a-5p and MCM2 was explored. Results showed miR-34a-5p expression in HCC tissues was significantly lower than in non HCC liver tissues (P < 0.05), but MCM2 expression in HCC tissues was markedly higher than in non HCC liver tissues (P < 0.05). In addition, miR-34a-5p expression was negatively related to MCM2 expression. To confirm effect of miR-34a-5p on tumor growth and its possible effect on MCM2, miR-34a-5p mimic and inhibitor was transfected into HCC cell lines (HepG2). MTS assay, showed miR-34a-5p over-expression could inhibit the proliferation of HCC cells. RT-qPCR was done to detect the expression of miR-34a-5p and MCM2 in HepG2 cells before and after transfection. Results showed that MCM2 expression in HCC tissues was markedly lower in mimic transfected group than in inhibitor transfected group and control group (P < 0.05) while miR-34a-5p expression in HepG2 cells was significantly higher in mimic transfected group than in inhibitor transfected group and control group (P < 0.05). Thus, miR-34a-5p may inhibit the proliferation of HCC cells via regulating MCM2 expression. These findings provide an evidence for the emerging role of microRNAs as diagnostic markers and therapeutic targets in HCC.

Wang P, Yan Y, Yu W, Zhang H
Role of ten-eleven translocation proteins and 5-hydroxymethylcytosine in hepatocellular carcinoma.
Cell Prolif. 2019; 52(4):e12626 [PubMed] Related Publications
In mammals, methylation of the 5th position of cytosine (5mC) seems to be a major epigenetic modification of DNA. This process can be reversed (resulting in cytosine) with high efficiency by dioxygenases of the ten-eleven translocation (TET) family, which perform oxidation of 5mC to 5-hydroxymethylcytosine (5hmC), 5-formylcytosine and 5-carboxylcytosine. It has been demonstrated that these 5mC oxidation derivatives are in a dynamic state and have pivotal regulatory functions. Here, we comprehensively summarized the recent research progress in the understanding of the physiological functions of the TET proteins and their mechanisms of regulation of DNA methylation and transcription. Among the three TET genes, TET1 and TET2 expression levels have frequently been shown to be low in hepatocellular carcinoma (HCC) tissues and received most attention. The modulation of TET1 also correlates with microRNAs in a post-transcriptional regulatory process. Additionally, recent studies revealed that global genomic 5hmC levels are down-regulated in HCC tissues and cell lines. Combined with the reported results, identification of 5hmC signatures in HCC tissues and in circulating cell-free DNA will certainly contribute to early detection and should help to design therapeutic strategies against HCC. 5hmC might also be a novel prognostic biomarker of HCC. Thus, a detailed understanding of the molecular mechanisms resulting in the premalignant and aggressive transformation of TET proteins and cells with 5hmC disruption might help to develop novel epigenetic therapies for HCC.

Gao S, Jiao B, Hong W, et al.
[Distribution of KIR/HLA alleles among ethnic Han Chinese patients with hepatocellular carcinoma from southern China].
Zhonghua Yi Xue Yi Chuan Xue Za Zhi. 2019; 36(5):439-442 [PubMed] Related Publications
OBJECTIVE: To assess the association of KIR/HLA alleles with hepatocellular carcinoma (HCC) and hepatitis B virus (HBV) infection among ethnic Han Chinese patients from southern China.
METHODS: For 95 patients with HCC and 171 healthy controls, the genotype of HLA-C alleles was determined with a PCR sequence-specific oligonucleotides typing method on an Illumina GenDx NGSgo platform. Genotypes comprised of HLA-C and KIR gene alleles were also subjected to statistical analysis.
RESULTS: In total 16 KIR genes (2DL2, 2DS2, 2DS3, 2DS5, 3DS1, 2DS1, 2DL5, 2DS4, 3DL1, 3DP1, 2DL3, 2DP1, 3DL3, 2DL1, 3DL2 and 2DL4) were discovered in the two groups. The frequencies of KIR2DL3 alleles and combinational genotypes of KIR2DL3/HLA-C1C2 were significantly lower in the patient group compared with the controls (0.9368 vs. 0.9883, χ²>3.84; P<0.05, OR = 0.1; 0.0112 vs. 0.2663, χ²>3.84; P<0.05, RR = 0.03). The frequency of HLA-C2C2 genotype of the patient group was significantly lower than that of the controls (0.0316 vs. 0.2690, P<0.05, RR = 0.09), while the frequency of HLA-C1C2 genotype was significantly higher than that of the controls (0.2316 vs. 0.0058, P<0.05, RR = 51.23).
CONCLUSION: Above results suggested that the KIR2DL3 allele is associated with lower risk for HCC. There may be individual difference in patients with HCC and HBV infection but various combinations of KIR/HLA alleles.

Li W, Liao X, Ning P, et al.
Paracrine effects of CCN3 from non-cancerous hepatic cells increase signaling and progression of hepatocellular carcinoma.
BMC Cancer. 2019; 19(1):395 [PubMed] Free Access to Full Article Related Publications
BACKGROUND: The liver microenvironment plays a key role in the progression and metastasis of hepatocellular carcinoma (HCC). Gene expression profiling of non-cancerous hepatic tissues obtained from patients with metastatic HCC exhibit a unique immune response signature, including upregulation of CCN3. However, the role of CCN3 secreted from non-cancerous hepatic tissues in the progression of HCC remains unclear.
METHODS: Using tissue microarrays, we examined CCN3 in non-cancerous hepatic tissues of patients with HCC and correlated expression with clinical and pathological features. In addition, CCN3 localization and mechanisms of HCC progression were investigated in tissues and cell lines. Finally, correlations between CCN3 and cirrhosis were explored in patients.
RESULTS: CCN3 was primarily localized to hepatic cells of non-cancerous hepatic tissues and was associated with vascular invasion and poor prognosis in patients with HCC. CCN3 expression in non-cancerous hepatic tissues also correlated with the degree of liver fibrosis. Compared with conditioned media from wild-type LO2 cells, conditioned media from hepatic cell line LO2 activated by LX2 (aLO2-CM) induced CCN3 expression and HCC cell proliferation and metastasis. Further, aLO2-CM activated MAPK signaling and epithelial-mesenchymal transition in HCC cells. Finally, CCN3 was inversely related to cirrhosis in the prognosis of HCC and negatively regulated hepatic stellate cells (HSCs) in vitro with downregulation of α-SMA, TGF-β, and collagens.
CONCLUSIONS: CCN3 was secreted from hepatic cells activated by HSCs and increased MAPK signaling, EMT, proliferation and metastasis of HCC cells. CCN3 was also inversely related to cirrhosis, regulating HSCs through a negative feedback loop.

Zhang C, Ge C
A Simple Competing Endogenous RNA Network Identifies Novel mRNA, miRNA, and lncRNA Markers in Human Cholangiocarcinoma.
Biomed Res Int. 2019; 2019:3526407 [PubMed] Free Access to Full Article Related Publications
Background: Cholangiocarcinoma (CCA) is the second most common malignant primary liver tumor and has shown an alarming increase in incidence over the last two decades. However, the mechanisms behind tumorigenesis and progression remain insufficient. The present study aimed to uncover the underlying regulatory mechanism on CCA and find novel biomarkers for the disease prognosis.
Method: The RNA-sequencing (RNA-seq) datasets of lncRNAs, miRNAs, and mRNAs in CCA as well as relevant clinical information were obtained from the Cancer Genome Atlas (TCGA) database. After pretreatment, differentially expressed RNAs (DERNAs) were identified and further interrogated for their correlations with clinical information. Prognostic RNAs were selected using univariate Cox regression. Then, a ceRNA network was constructed based on these RNAs.
Results: We identified a total of five prognostic DEmiRNAs, 63 DElncRNAs, and 90 DEmRNAs between CCA and matched normal tissues. Integrating the relationship between the different types of RNAs, an lncRNA-miRNA-mRNA network was established and included 28 molecules and 47 interactions. Screened prognostic RNAs involved in the ceRNA network included 3 miRNAs (hsa-mir-1295b, hsa-mir-33b, and hsa-mir-6715a), 7 lncRNAs (ENSG00000271133, ENSG00000233834, ENSG00000276791, ENSG00000241155, COL18A1-AS1, ENSG00000274737, and ENSG00000235052), and 18 mRNAs (ANO9, FUT4, MLLT3, ABCA3, FSCN2, GRID2IP, NCK2, MACC1, SLC35E4, ST14, SH2D3A, MOB3B, ACTL10, RAB36, ATP1B3, MST1R, SEMA6A, and SEL1L3).
Conclusions: Our study identified novel prognostic makers and predicted a previously unknown ceRNA regulatory network in CCA and may provide novel insight into a further understanding of lncRNA-mediated ceRNA regulatory mechanisms in CCA.

Kim E, Lisby A, Ma C, et al.
Promotion of growth factor signaling as a critical function of β-catenin during HCC progression.
Nat Commun. 2019; 10(1):1909 [PubMed] Free Access to Full Article Related Publications
Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related deaths worldwide. β-catenin is widely thought to be a major oncogene in HCC based on the frequency of mutations associated with aberrant Wnt signaling in HCC patients. Challenging this model, our data reveal that β-catenin nuclear accumulation is restricted to the late stage of the disease. Until then, β-catenin is primarily located at the plasma membrane in complex with multiple cadherin family members where it drives tumor cell survival by enhancing the signaling of growth factor receptors such as EGFR. Therefore, our study reveals the evolving nature of β-catenin in HCC to establish it as a compound tumor promoter during the progression of the disease.

Lu W, Yang C, Du P, et al.
Expression tendency and prognostic value of TCF21 in hepatocellular carcinoma.
Artif Cells Nanomed Biotechnol. 2019; 47(1):1466-1470 [PubMed] Related Publications
BACKGROUND: Transcription factor 21 (TCF21) is identified as a tumor suppressor in a variety of human tumors. The purpose of the study was to examine its expression tendency and prognostic value in hepatocellular carcinoma (HCC).
METHODS: Relative expression of TCF21 mRNA in tissue samples from HCC patients and healthy volunteers were detected through quantitative real-time polymerase chain reaction (qRT-PCR) while its protein level was examined via immunohistochemistry analysis. Chi-square test was adopted to assess the association of TCF21 expression with the clinicopathological characteristic of the patients. Then Kaplan-Meier analysis was employed to analyze the function of TCF21 expression on overall survival among HCC patients.
RESULTS: Both the mRNA and protein levels of TCF21 were significantly reduced in HCC tissue samples compared with healthy controls (p < .05). Also, its expression was obviously affected by the classification of tissue pathology, metastasis, T stage, N stage and pathological grading. According to Kaplan-Meier analysis, patients with higher expression of TCF21 experienced dramatically longer overall survival time than those with lower expression (log rank test, p < .001).
CONCLUSIONS: TCF21 expression was decreased in HCC patients and it could act as a prognostic marker.

Song W, Gu Y, Lu S, et al.
LncRNA TRERNA1 facilitates hepatocellular carcinoma metastasis by dimethylating H3K9 in the CDH1 promoter region via the recruitment of the EHMT2/SNAI1 complex.
Cell Prolif. 2019; 52(4):e12621 [PubMed] Related Publications
OBJECTIVES: Long non-coding RNAs (LncRNAs) play an important role in hepatocellular carcinoma development, however, as a crucial driver of hepatocellular carcinoma (HCC) metastasis, their functions in tumour metastasis remain largely unknown.
MATERIALS AND METHODS: The lncRNA TRERNA1 expression levels were detected in HCC by quantitative real-time PCR (qPCR). The function of TRERNA1 was examined by wound-healing assays, transwell assays and tail vein injection experiments. The potential regulatory mechanisms of TRERNA1 on its target genes were explored by ChIP, RIP, IP and WB assays.
RESULTS: Elevated TRERNA1 levels promoted HCC cell migration and invasion in vitro and in vivo. TRERNA1 recruited EHMT2 to dimethylate H3K9 in the CDH1 promoter region. Furthermore, EHMT2 bound to SNAI1 to suppress CDH1 expression in HCC cells. After inhibiting TRERNA1, the expression level of CDH1 was restored and was involved in the regulation of the EHMT2/SNAI1 complex. The level of TRERNA1 was positively correlated with tumour metastasis and was negatively correlated with the expression of CDH1 in HCC tissues.
CONCLUSIONS: For the first time, the current study reveals that TRERNA1 promotes cell metastasis and the invasion of HCC via the recruitment of EHMT2 and/or the EHMT2/SNAI1 complex to suppress CDH1. These data identify a novel mechanism that regulates TRERNA1 in metastatic HCC and provides a potential targeted therapy for HCC patients.

Xu J, Wang X, Yan C, Chen W
A Polyamidoamine Dendrimer-Based Electrochemical Immunosensor for Label-Free Determination of Epithelial Cell Adhesion Molecule- Expressing Cancer Cells.
Sensors (Basel). 2019; 19(8) [PubMed] Free Access to Full Article Related Publications
A new electrochemical immunosensor for cancer cell detection based on a specific interaction between the metastasis-related antigen of epithelial cell adhesion molecule (EpCAM) on the cell membrane and its monoclonal antibody (Anti-EpCAM) immobilized on a gold electrode has been developed. The amino-terminated polyamidoamine dendrimer (G6 PAMAM) was first covalently attached to the 3-mercaptopropionic acid (MPA)-functionalized gold electrode to obtain a thin film, and then completely carboxylated by succinic anhydride (SA). Next, the Anti-EpCAM was covalently bound with the G6 PAMAM to obtain a stable recognition layer. In the presence of the EpCAM expressing hepatocellular carcinomas cell line of HepG2, the specific immune recognition (Anti-EpCAM/EpCAM) led to an obvious change of the electron transfer ability. The properties of the layer-by-layer assembly process was examined by cyclic voltammetry (CV) and electrochemical impedance spectroscopy (EIS). The final determination of HepG2 cells was performed in the presence of the reversible [Fe(CN)

Yu D, Zhao J, Wang Y, et al.
Upregulated histamine receptor H3 promotes tumor growth and metastasis in hepatocellular carcinoma.
Oncol Rep. 2019; 41(6):3347-3354 [PubMed] Related Publications
Histamine receptor H3 (HRH3) is mainly expressed in the central nervous system, where it is involved in the regulation of the release of various neurotransmitters in the brain. Recent studies have demonstrated that the expression of HRH3 is upregulated in several types of cancer. However, the functional effect of HRH3 on tumor progression remains largely unknown, particularly in hepatocellular carcinoma (HCC). In the present study, the expression of HRH3 in 96 HCC patients was first evaluated, and its clinical significance was analyzed. Subsequently, the functional roles of HRH3 in HCC growth and metastasis were systematically explored in vitro and in vivo using its agonist (imetit) or antagonist (clobenpropit). It was observed that HRH3 was significantly upregulated in HCC tissues, while its expression was significantly associated with recurrence‑free survival and overall survival in HCC patients. Functional experiments also demonstrated that HRH3 upregulation facilitated the growth and metastasis of HCC cells by inducing the formation of lamellipodia. These findings revealed that HRH3 serves an important role in the growth and metastasis of HCC cells, which provides experimental evidence supporting the application of HRH3 as a potential therapeutic target in HCC treatment.

Zhu X, Qin M, Li C, et al.
Downregulated Expression of Chromobox Homolog 7 in Hepatocellular Carcinoma.
Genet Test Mol Biomarkers. 2019; 23(5):348-352 [PubMed] Related Publications

Kong Q, Liang C, Jin Y, et al.
The lncRNA MIR4435-2HG is upregulated in hepatocellular carcinoma and promotes cancer cell proliferation by upregulating miRNA-487a.
Cell Mol Biol Lett. 2019; 24:26 [PubMed] Free Access to Full Article Related Publications
Background: Given the high mortality rate and unclear pathogenesis for liver cancer, investigation of its molecular mechanisms is essential. We focused on the long non-coding RNA (lncRNA) MIR4435-2HG, which was recently reported to be oncogenic in lung cancer and the microRNA miRNA-487a, which has been reported to be oncogenic in hepatocellular carcinoma (HCC). Our aim was to determine if the former has a role in HCC, and to further validate the role of the latter.
Methods: Samples from 64 patients with HCC were taken at The Third Affiliated Hospital of Sun Yat-Sen University. Cell transfection and PCR were applied.
Results: We found that MIR4435-2HG and miRNA-487a were upregulated in tumor tissues compared to adjacent healthy tissues from HCC patients. The expression of MIR4435-2HG was significantly affected by tumor size but not by tumor metastasis. Correlation analysis showed that MIR4435-2HG and miRNA-487a were positively correlated in both the tumor tissues and adjacent healthy tissues from HCC patients. Overexpression of MIR4435-2HG led to upregulation of miRNA-487a in the cells of HCC cell lines, while overexpression of miRNA-487a did not significantly affect MIR4435-2HG. Overexpression of MIR4435-2HG and miRNA-487a promoted the proliferation of cells of HCC cell lines, and miRNA-487a knockdown partially attenuated the enhancing effects of MIR4435-2HG overexpression on cancer cell proliferation.
Conclusion: MIR4435-2HG is upregulated in HCC and promotes cancer cell proliferation possibly by upregulating miRNA-487a.

Wu Y, Yang X, Chen Z, et al.
m
Mol Cancer. 2019; 18(1):87 [PubMed] Free Access to Full Article Related Publications
BACKGROUND: Long noncoding RNAs (lncRNAs) have emerged as critical players in cancer progression, but their functions in colorectal cancer (CRC) metastasis have not been systematically clarified.
METHODS: lncRNA expression profiles in matched normal and CRC tissue were checked using microarray analysis. The biological roles of a novel lncRNA, namely RP11-138 J23.1 (RP11), in development of CRC were checked both in vitro and in vivo. Its association with clinical progression of CRC was further analyzed.
RESULTS: RP11 was highly expressed in CRC tissues, and its expression increased with CRC stage in patients. RP11 positively regulated the migration, invasion and epithelial mesenchymal transition (EMT) of CRC cells in vitro and enhanced liver metastasis in vivo. Post-translational upregulation of Zeb1, an EMT-related transcription factor, was essential for RP11-induced cell dissemination. Mechanistically, the RP11/hnRNPA2B1/mRNA complex accelerated the mRNA degradation of two E3 ligases, Siah1 and Fbxo45, and subsequently prevented the proteasomal degradation of Zeb1. m
CONCLUSIONS: m

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