Gene Summary

Gene:WNT3A; Wnt family member 3A
Summary:The WNT gene family consists of structurally related genes which encode secreted signaling proteins. These proteins have been implicated in oncogenesis and in several developmental processes, including regulation of cell fate and patterning during embryogenesis. This gene is a member of the WNT gene family. It encodes a protein which shows 96% amino acid identity to mouse Wnt3A protein, and 84% to human WNT3 protein, another WNT gene product. This gene is clustered with WNT14 gene, another family member, in chromosome 1q42 region. [provided by RefSeq, Jul 2008]
Databases:OMIM, HGNC, Ensembl, GeneCard, Gene
Protein:protein Wnt-3a
Source:NCBIAccessed: 01 September, 2019


What does this gene/protein do?
Show (77)
Pathways:What pathways are this gene/protein implicaed in?
Show (2)

Cancer Overview

Research Indicators

Publications Per Year (1994-2019)
Graph generated 01 September 2019 using data from PubMed using criteria.

Literature Analysis

Mouse over the terms for more detail; many indicate links which you can click for dedicated pages about the topic.

Tag cloud generated 01 September, 2019 using data from PubMed, MeSH and CancerIndex

Specific Cancers (6)

Data table showing topics related to specific cancers and associated disorders. Scope includes mutations and abnormal protein expression.

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

Latest Publications: WNT3A (cancer-related)

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.

Lyu X, Wang L, Lu J, et al.
microRNA‑485 inhibits the malignant behaviors of retinoblastoma by directly targeting Wnt3a.
Oncol Rep. 2019; 41(5):3137-3147 [PubMed] Related Publications
Deregulation of microRNAs (miRNAs) has been widely reported in retinoblastoma (RB), and the aberrantly expressed miRNAs may serve as crucial epigenetic regulators in the occurrence and development of RB. Therefore, the identification of dysregulated miRNAs in RB may be useful for the development of effective targets for the therapy patients with this disease. miRNA (miR)‑485‑5p (miR‑485) is deregulated in multiple human cancer types and serves crucial roles in their progression and development. However, the expression pattern of miR‑485 and its role in RB have not been well investigated. In the present study, expression levels of miR‑485 in RB tissues and cell lines were measured using reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). The effects of miR‑485 overexpression on RB cell proliferation, apoptosis, migration and invasion were examined using Cell Counting Kit‑8 assay, flow cytometric analysis and in vitro migration and invasion assays, respectively. Xenograft tumor formation assay was utilized to determine the influence of miR‑485 on RB tumor growth in vivo. The mechanism responsible for the tumor‑suppressing roles of miR‑485 in RB progression was determined through a series of experiments, including bioinformatics prediction, luciferase reporter assay, RT‑qPCR, western blot analysis and rescue experiments. Herein, a marked downregulation of miR‑485 expression in human RB tissues and cell lines was observed. miR‑485 overexpression suppressed RB cell proliferation, induced cell apoptosis, attenuated cell migration and cell invasion in vitro, and restrained the growth of RB cells in vivo. Additionally, Wnt3a was revealed to be a direct target gene of miR‑485 in RB cells. Wnt3a was upregulated in human RB tissues, and its upregulation was inversely associated with miR‑485. Furthermore, the tumor suppressive roles of Wnt3a silencing were similar to those of miR‑485 overexpression in RB cells. In addition, restoration of Wnt3a expression partially reversed the tumor suppressor action of miR‑485 in RB cells. However, miR‑485 upregulation directly targeted Wnt3a to inhibit activation of the Wnt/β‑catenin signaling pathway in RB cells both in vitro and in vivo. Notably, these results demonstrated that the tumor‑suppressive roles of miR‑485 were at least partially mediated by Wnt3a in RB cells. Therefore, miR‑485 is a potential therapeutic target for treating patients with RB.

Götzel K, Chemnitzer O, Maurer L, et al.
In-depth characterization of the Wnt-signaling/β-catenin pathway in an in vitro model of Barrett's sequence.
BMC Gastroenterol. 2019; 19(1):38 [PubMed] Free Access to Full Article Related Publications
BACKGROUND: An altered Wnt-signaling activation has been reported during Barrett's esophagus progression, but with rarely detected mutations in APC and β-catenin (CTNNB1) genes.
METHODS: In this study, a robust in-depth expression pattern analysis of frizzled receptors, co-receptors, the Wnt-ligands Wnt3a and Wnt5a, the Wnt-signaling downstream targets Axin2, and CyclinD1, as well as the activation of the intracellular signaling kinases Akt and GSK3β was performed in an in vitro cell culture model of Barrett's esophagus. Representing the Barrett's sequence, we used normal esophageal squamous epithelium (EPC-1, EPC-2), metaplasia (CP-A) and dysplasia (CP-B) to esophageal adenocarcinoma (EAC) cell lines (OE33, OE19) and primary specimens of squamous epithelium, metaplasia and EAC.
RESULTS: A loss of Wnt3a expression was observed beginning from the metaplastic cell line CP-A towards dysplasia (CP-B) and EAC (OE33 and OE19), confirmed by a lower staining index of WNT3A in Barrett's metaplasia and EAC, than in squamous epithelium specimens. Frizzled 1-10 expression analysis revealed a distinct expression pattern, showing the highest expression for Fzd2, Fzd3, Fzd4, Fzd5, Fzd7, and the co-receptor LRP5/6 in EAC cells, while Fzd3 and Fzd7 were rarely expressed in primary specimens from squamous epithelium.
CONCLUSION: Despite the absence of an in-depth characterization of Wnt-signaling-associated receptors in Barrett's esophagus, by showing variations of the Fzd- and co-receptor profiles, we provide evidence to have a significant role during Barrett's progression and the underlying pathological mechanisms.

Lu H, Ju DD, Yang GD, et al.
Targeting cancer stem cell signature gene SMOC-2 Overcomes chemoresistance and inhibits cell proliferation of endometrial carcinoma.
EBioMedicine. 2019; 40:276-289 [PubMed] Free Access to Full Article Related Publications
BACKGROUND: Endometrial cancer is one of the most common gynecological malignancies and has exhibited an increasing incidence rate in recent years. Cancer stem cells (CSCs), which are responsible for tumor growth and chemoresistance, have been confirmed in endometrial cancer. However, it is still challenging to identify endometrial cancer stem cells to then target for therapy.
METHODS: Flow cytometry was used to identify the endometrial cancer stem cells. Sphere formation assay, western blotting, qRT-PCR assay, cell viability assay, xenograft assay and immunohistochemistry staining analysis were utilized to evaluate the effect of SPARC-related modular calcium binding 2 (SMOC-2) on the cells proliferation and drug resistance. Cell viability assay, qRT-PCR assay, immunofluorescence staining, Co-IP assay and luciferase reporter gene assay were performed to explore the possible molecular mechanism by which SMOC-2 activates WNT/β-catenin pathway.
FINDINGS: We found the expression of SPARC-related modular calcium binding 2 (SMOC-2), a member of SPARC family, was higher in endometrial CSCs than that in non-CSCs. SMOC-2 was also more highly expressed in spheres than in monolayer cultures. The silencing of SMOC-2 suppressed cell sphere ability; reduced the expression of the stemness-associated genes SOX2, OCT4 and NANOG; and enhanced chemosensitivity in endometrial cancer cells. By co-culture IP assay, we demonstrated that SMOC-2 directly interacted with WNT receptors (Fzd6 and LRP6), enhanced ligand-receptor interaction with canonical WNT ligands (Wnt3a and Wnt10b), and finally, activated the WNT/β-catenin pathway in endometrial cancer. SMOC-2 expression was closely correlated with CSC markers CD133 and CD44 expression in endometrial cancer tissue.
INTERPRETATION: Taken together, we conclude that SMOC-2 might be a novel endometrial cancer stem cell signature gene and therapeutic target for endometrial cancer. FUND: National Natural Science Foundation of China, Scientific and Technological Innovation Act Program of Shanghai Science and Technology Commission, Scientific and Technological Innovation Act Program of Fengxian Science and Technology Commission, Natural Science Foundation of Shanghai.

de Freitas EM, Machado RA, de Moura Santos E, et al.
Polymorphisms associated with oral clefts as potential susceptibility markers for oral and breast cancer.
Arch Oral Biol. 2019; 99:9-14 [PubMed] Related Publications
OBJECTIVE: To evaluate the association of single nucleotide polymorphisms (SNPs) in genes/loci consistently altered in nonsyndromic oral clefts in patients with oral and breast cancer in a Brazilian population.
DESIGN: This case-control study evaluated the association of SNPs in IRF6 (rs642961), WNT3A (rs708111), GSK3β (rs9879992), 8q24 (rs987525) and WNT11 (rs1533767), representing regions consistently identified as of susceptibility for oral clefts, with oral cancer (oral squamous cell carcinoma) and breast cancer. Logistic regression analyses were used for confounding adjustments, and p values ≤0.01 were considered statistically significant (Bonferroni correction = 0.05/5 polymorphic markers).
RESULTS: The minor G allele of rs9879992 in GSK3β was associated with oral cancer risk (p = 0.02), whereas rs1533767 in WNT11 showed a protective effect against it (p = 0.04). Several SNP-SNP interactions containing GSK3β rs9879992 were significantly associated with oral cancer after 1000 permutation test. To breast cancer, the A allele of rs987525 was associated with increase risk in early stage (p = 0.02) and SNP-SNP interactions involving the 5 SNPs were significantly observed, with the most significant interaction among rs708111, rs1533767, rs9879992 and rs642961 (p
CONCLUSION: Our results reveal associations of SNPs consistently altered in oral cleft with oral and breast cancer risk, raising interesting possibilities to identify risk markers for those tumors.

Fan X, Huang X, Li Z, Ma X
MicroRNA-372-3p promotes the epithelial-mesenchymal transition in breast carcinoma by activating the Wnt pathway.
J BUON. 2018 Sep-Oct; 23(5):1309-1315 [PubMed] Related Publications
PURPOSE: To explore the role of microRNA (miR)-372-3p in the epithelial-mesenchymal transition (EMT) of breast carcinoma and its potential mechanism.
METHODS: The expression of miR-372-3p was detected by real-time PCR (RT-PCR) in 48 samples of breast carcinoma tissues, 30 samples of normal breast tissues, normal breast cells (MCF-10A) and breast carcinoma cells (MCF-7, MDA-MB-231 and HCC38). Transfection efficacy of miR-372-3p mimic and miR-372-3p inhibitor was determined by RT-PCR. Cell viability and invasion were determined by CCK-8 assay and wound healing assay, respectively. The interaction between miR-372-3p and DDK1 was verified by the luciferase reporter assay. Expression levels of DDK1, Wnt3a, E-cadherin and N-cadherin in breast carcinoma cells transfected with miR-372-3p mimic, miR-372-3p inhibitor and DKK1 were detected by Western blot.
RESULTS: The expression of miR-372-3p in breast carcinoma tissues was higher than that of normal breast tissues. Correlation analysis revealed that the miR-372-3p expression was negatively correlated with the postoperative survival, but positively correlated with the tumor size and stage of patients with breast carcinoma. No significant correlation was observed between the miR-372-3p expression and age, gender or lymph node metastasis. The receiver operating characteristics (ROC) curve indicated a high diagnostic sensitivity and specificity for miR-372-3p. CCK-8 assay and wound healing assay illustrated that miR-372-3p increased the viability and invasion of MDA-MB-231 and HCC38 cells, respectively. Luciferase activity assay suggested that miR-372-3p was specifically bound to the 3'UTR of DKK1. Overexpressed miR-372-3p markedly increased the expressions of Wnt3a and N-cadherin, but decreased the expressions of DKK1 and E-cadherin, which were reversed by miR-372-3p knockdown. The protein expressions of E-cadherin and N-cadherin were remarkably increased in cells co-transfected with miR-372-3p mimic and DKK1 in comparison with those transfected with miR-372-3p mimic only.
CONCLUSIONS: MiR-372-3p is upregulated in breast carcinoma tissues, which promotes the viability and invasion of breast carcinoma cells through the Wnt pathway.

Zhu Z, Wei D, Li X, et al.
RNA-binding protein QKI regulates contact inhibition via Yes-associate protein in ccRCC.
Acta Biochim Biophys Sin (Shanghai). 2019; 51(1):9-19 [PubMed] Related Publications
Contact inhibition adjusts organ size to the proper size and ensures the cultured cells growing to a monolayer. By regulating the downstream coordinator YAP, the evolutionarily conserved Hippo transduction pathway attunes cell growth and death in response to cell contact inhibition, polarity, self-renewal, and differentiation. Dysregulation of this pathway is involved in various diseases such as cancer. RNA-binding protein QKI regulates cell proliferation, metabolism, division, and immunity in various cancer models, but its role in cancer cell contact inhibition remains unclear. In this study, we aimed to clarify the relationship between QKI and YAP, and the role of their interaction in cell contact inhibition. We found a lower QKI expression level in sparse condition, whereas a higher expression level in confluent condition by western blot analysis and immunofluorescence assay. QKI knockdown elevated cell proliferation and invasion both in vitro and in vivo. Strikingly, the results of CCK-8 assay, colony formation assay, and transwell assay showed that the phenomenon was in accord with the expression level of pYAP and reverse with YAP. Higher levels of Wnt3a and β-catenin were also found in xenografts of QKI-knockdown clear cell renal cell carcinoma (ccRCC) CAKI-1 cells by western blot analysis and immumohistochemical staining. Finally, a positive correlation between QKI and pYAP was found in clinical specimens by immunohistochemistry. Thus, as a negative regulator of YAP, QKI attuned the cell contact inhibition, leading to inhibition of cancer cell proliferation and invasion through Wnt and GPCR pathway.

Wang Y, Yang Q, Cheng Y, et al.
Myosin Heavy Chain 10 (MYH10) Gene Silencing Reduces Cell Migration and Invasion in the Glioma Cell Lines U251, T98G, and SHG44 by Inhibiting the Wnt/β-Catenin Pathway.
Med Sci Monit. 2018; 24:9110-9119 [PubMed] Free Access to Full Article Related Publications
BACKGROUND The myosin heavy chain 10 or MYH10 gene encodes non-muscle myosin II B (NM IIB), and is involved in tumor cell migration, invasion, extracellular matrix (ECM) production, and epithelial-mesenchymal transition (EMT). This study aimed to investigate the effects of the MYH10 gene on normal human glial cells and glioma cell lines in vitro, by gene silencing, and to determine the signaling pathways involved. MATERIAL AND METHODS The normal human glial cell line HEB, and the glioma cell lines, U251, T98G, and SHG44 were studied. Plasmid transfection silenced the MYH10 gene. The cell counting kit-8 (CCK-8) assay evaluated cell viability. Cell migration and invasion were evaluated using scratch and transwell assays. Western blot measured the protein expression levels, and quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the mRNA expression levels, for MYH10, metastasis-associated protein 1 (MTA-1), matrix metalloproteinase (MMP)-1, MMP-9, tissue inhibitor of metalloproteinases 2 (TIMP2), collagen 1, E-cadherin, vimentin, Wnt3a, β-catenin, and cyclin D1. RESULTS The MYH10 gene was overexpressed in U251, T98G, and SHG44 cells. MYH10 expression was down-regulated following siMYH10 plasmid interference, which also inhibited glioma cell migration and invasion. MYH10 gene silencing resulted in reduced expression of MTA-1, MPP-2, MMP-9 and vimentin, and increased expression of TIMP-2, E-cadherin and collagen 1 at the protein and mRNA level, and inhibited the Wnt/β-catenin pathway. CONCLUSIONS In human glioma cell lines, silencing the MYH10 gene reduced cell migration and invasion, by inhibiting the Wnt/β-catenin pathway, which may regulate the ECM and inhibit EMT in human glioma.

Li J, Fang R, Wang J, Deng L
NOP14 inhibits melanoma proliferation and metastasis by regulating Wnt/β-catenin signaling pathway.
Braz J Med Biol Res. 2018; 52(1):e7952 [PubMed] Free Access to Full Article Related Publications
Malignant melanoma is an aggressive skin cancer with a high mortality rate. Nucleolar protein 14 (NOP14) has been implicated in cancer development. However, the role of NOP14 in malignant melanoma progression remains largely unclear. In this study, we observed that malignant melanoma tissue showed NOP14 down-regulation compared to melanocytic nevi tissues. Moreover, we observed that NOP14 expression was significantly associated with melanoma tumor thickness and lymph node metastasis. NOP14 overexpression in melanoma cells suppressed proliferation, caused G1 phase arrest, promoted apoptosis, and inhibited melanoma cell migration and invasion. Further investigations revealed that NOP14 overexpression reduced the expression levels of Wnt3a, β-catenin, and GSK-3β of the Wnt/β-catenin pathway. In summary, we demonstrated that NOP14 inhibited melanoma cell proliferation and metastasis by regulating the Wnt/β-catenin signaling pathway.

Le PN, Keysar SB, Miller B, et al.
Wnt signaling dynamics in head and neck squamous cell cancer tumor-stroma interactions.
Mol Carcinog. 2019; 58(3):398-410 [PubMed] Article available free on PMC after 01/03/2020 Related Publications
Wnt pathway activation maintains the cancer stem cell (CSC) phenotype and promotes tumor progression, making it an attractive target for anti-cancer therapy. Wnt signaling at the tumor and tumor microenvironment (TME) front have not been investigated in depth in head and neck squamous cell carcinoma (HNSCC). In a cohort of 48 HNSCCs, increased Wnt signaling, including Wnt genes (AXIN2, LGR6, WISP1) and stem cell factors (RET, SOX5, KIT), were associated with a more advanced clinical stage. Key Wnt pathway proteins were most abundant at the cancer epithelial-stromal boundary. To investigate these observations, we generated three pairs of cancer-cancer associated fibroblast (CAF) cell lines derived from the same HNSCC patients. 3D co-culture of cancer spheres and CAFs mimicked these in vivo interactions, and using these we observed increased expression of Wnt genes (eg, WNT3A, WNT7A, WNT16) in both compartments. Of these Wnt ligands, we found Wnt3a, and less consistently Wnt16, activated Wnt signaling in both cancer cells and CAFs. Wnt activation increased CSC characteristics like sphere formation and invasiveness, which was further regulated by the presence of CAFs. Time lapse microscopy also revealed preferential Wnt activation of cancer cells. Wnt inhibitors, OMP-18R5 and OMP-54F28, significantly reduced growth of HNSCC patient-derived xenografts and suppressed Wnt activation at the tumor epithelial-stromal boundary. Taken together, our findings suggest that Wnt signaling is initiated in cancer cells which then activate CAFs, and in turn perpetuate a paracrine signaling loop. This suggests that targeting Wnt signaling in the TME is essential.

Liu SQ, Zhang JL, Li ZW, et al.
Propofol Inhibits Proliferation, Migration, Invasion and Promotes Apoptosis Through Down-Regulating miR-374a in Hepatocarcinoma Cell Lines.
Cell Physiol Biochem. 2018; 49(6):2099-2110 [PubMed] Related Publications
BACKGROUND: Propofol is a commonly used anaesthetic with controversial effects on cancer cells. We aimed to explore the functional roles of propofol in hepatocellular carcinoma (HCC) cells as well as the underlying mechanisms.
METHODS: HepG2 and SMMC-7721 cells were used in this study. Firstly, the effects of propofol on cell viability, migration, invasion, apoptosis, and involved proteins were assessed by Cell Counting Kit-8 assay, Transwell assay, flow cytometry assay and Western blot analysis, respectively. Subsequently, alteration of miR-374a after stimulation of propofol was analyzed by qRT-PCR. miR-374a was overexpressed and the alteration of proteins in the Wnt/β-catenin and PI3K/AKT pathways was detected by Western blot analysis. The downstream factor of miR-374a was finally studied.
RESULTS: Propofol inhibited cell viability, migration and invasion but promoted apoptosis of HepG2 and SMMC-7721 cells. Meanwhile, cyclinD1, matrix metalloproteinase (MMP)-2 and MMP-9 were down-regulated while Bax/Bcl-2, cleaved caspase-3 and cleaved caspase-9 were up-regulated by propofol. Then, miR-374a level was reduced by propofol. Expression of Wnt3a, β-catenin, p-PI3K and p-AKT was decreased by propofol, whereas these decreases were reversed by miR-374a overexpression. Finally, TP53 was proven to be target of miR-374a in HepG2 cells.
CONCLUSION: Propofol inhibited cell proliferation, migration and invasion while promoted cell apoptosis of HepG2 and SMMC-7721 cells through inhibiting the Wnt/β-catenin and PI3K/ AKT pathways via down-regulation of miR-374a. Besides, miR-374a affected propofol-treated HepG2 cells by targeting TP53.

Hwang SM, Lee HJ, Jung JH, et al.
Inhibition of Wnt3a/FOXM1/β-Catenin Axis and Activation of GSK3β and Caspases are Critically Involved in Apoptotic Effect of Moracin D in Breast Cancers.
Int J Mol Sci. 2018; 19(9) [PubMed] Article available free on PMC after 01/03/2020 Related Publications
Although Moracin D derived from

Lu F, Ye Y, Zhang H, et al.
miR-497/Wnt3a/c-jun feedback loop regulates growth and epithelial-to-mesenchymal transition phenotype in glioma cells.
Int J Biol Macromol. 2018; 120(Pt A):985-991 [PubMed] Related Publications
Glioma is one of the most frequent intracranial malignant tumors. Abnormal expression of microRNAs usually contributes to the development and progression of glioma. In the current study, we explored the role and underlying mechanism of miR-497 in glioma. We revealed that miR-497 expression was significantly down-regulated in glioma tissues and cell lines. Reduced expression of miR-497 was associated with poor disease-free and over-all survival rate. Restoration of miR-497 decreased glioma cell growth and invasion both in vitro and in vivo. The oncogene Wnt3a was identified as a downstream target of miR-497 by using luciferase and western blot assays. Knockdown of Wnt3a mimicked the effect of miR-497 in glioma cells. In summary, our study demonstrated that miR-497 may function as a tumor suppressor in glioma and suggested that miR-497 is a potential therapeutic target for glioma patients.

Prossomariti A, Piazzi G, D'Angelo L, et al.
miR-155 Is Downregulated in Familial Adenomatous Polyposis and Modulates WNT Signaling by Targeting AXIN1 and TCF4.
Mol Cancer Res. 2018; 16(12):1965-1976 [PubMed] Related Publications
Adenomatous Polyposis Coli (

Matias D, Dubois LG, Pontes B, et al.
GBM-Derived Wnt3a Induces M2-Like Phenotype in Microglial Cells Through Wnt/β-Catenin Signaling.
Mol Neurobiol. 2019; 56(2):1517-1530 [PubMed] Related Publications
Glioblastoma is an extremely aggressive and deadly brain tumor known for its striking cellular heterogeneity and capability to communicate with microenvironment components, such as microglia. Microglia-glioblastoma interaction contributes to an increase in tumor invasiveness, and Wnt signaling pathway is one of the main cascades related to tumor progression through changes in cell migration and invasion. However, very little is known about the role of canonical Wnt signaling during microglia-glioblastoma crosstalk. Here, we show for the first time that Wnt3a is one of the factors that regulate interactions between microglia and glioblastoma cells. Wnt3a activates the Wnt/β-catenin signaling of both glioblastoma and microglial cells. Glioblastoma-conditioned medium not only induces nuclear translocation of microglial β-catenin but also increases microglia viability and proliferation as well as Wnt3a, cyclin-D1, and c-myc expression. Moreover, glioblastoma-derived Wnt3a increases microglial ARG-1 and STI1 expression, followed by an upregulation of IL-10 mRNA levels, and a decrease in IL1β gene expression. The presence of Wnt3a in microglia-glioblastoma co-cultures increases the formation of membrane nanotubes accompanied by changes in migration capability. In vivo, tumors formed from Wnt3a-stimulated glioblastoma cells presented greater microglial infiltration and more aggressive characteristics such as growth rate than untreated tumors. Thus, we propose that Wnt3a belongs to the arsenal of factors capable of stimulating the induction of M2-like phenotype on microglial cells, which contributes to the poor prognostic of glioblastoma, reinforcing that Wnt/β-catenin pathway can be a potential therapeutic target to attenuate glioblastoma progression.

Li B, Wang S, Wang S
MiR-195 suppresses colon cancer proliferation and metastasis by targeting WNT3A.
Mol Genet Genomics. 2018; 293(5):1245-1253 [PubMed] Related Publications
MicroRNAs (miRNAs) are a novel class of diagnostic and therapeutic target in cancer. Here, we aimed to explore the effects and mechanism of miR-195 regulation in colon cancer. The expressions of several putative miRNAs in colon tumors, compared to those in normal tissues, were investigated by bioinformatical analysis of a Gene Expression Omnibus database. Quantitative real-time PCR analysis (qRT-PCR) was used to validate the identified changes in normal tissues, primary tumors, and metastatic tumors. MTT, soft agar colony formation, and transwell assays were used to evaluate the effects of miR-195 overexpression or inhibition on cell viability, proliferation, migration, and invasion. Targets of miR-195 were identified by TargetScan, and subsequently verified by qRT-PCR and Western blot. The role of miR-195 in the β-catenin pathway was also studied using RT-PCR and Western blot. MiR-195 expression was downregulated in colon carcinoma tissues and negatively correlated with the metastatic potential. While transfecting miR-195 mimics decreased the proliferation, migration, and invasion of colon cancer cells, miR-195 inhibition exerted opposing effects. WNT3A was identified as a direct target of miR-195. β-catenin was also downregulated by miR-195 in colon cancers. MiR-195 downregulation is associated with the enhanced proliferation, migration, and invasion of colon cancer. MiR-195 directly downregulates WNT3A. Our results indicate that miR-195 is a potential diagnostic marker and therapeutic target for improving the clinical management of colon cancer.

Marimuthu M, Andiappan M, Wahab A, et al.
Canonical Wnt pathway gene expression and their clinical correlation in oral squamous cell carcinoma.
Indian J Dent Res. 2018 May-Jun; 29(3):291-297 [PubMed] Related Publications
Aim: The aim of this study is to explore the prognostic significance and clinicopathological correlations of the Wnt pathway genes in a cohort of surgically treated patients with oral squamous cell carcinoma (OSCC) patients.
Settings and Design: A prospective genetic study on patients with OSCC was carried out during the period from July 2014 to January 2016. Informed consent from patients and institutional ethical approval for the study was obtained and the guidelines were strictly followed for collection of samples.
Subjects and Methods: Clinical data and mRNA expression analysis of ten genes in the canonical Wnt pathway were evaluated and their relationships with clinical and demographic variables were studied in 58 tissue samples. Wnt-3a, β-catenin, secreted frizzled-related proteins sFRP-1, sFRP-2, sFRP-4, sFRP-5, Wnt inhibitory factor 1, dickkopf-1, c-MYC, and cyclin-D1 from cancer (n = 29) and normal (n = 29) tissue samples were investigated using quantitative reverse transcription-polymerase chain reaction.
Statistical Analysis: Descriptive statistics were used to summarize the sample characteristics and clinical variables. If the data were normal, then parametric tests were used; otherwise, nonparametric alternatives were used. All the analyses were carried out using SPSS version 23.0 (IBM SPSS Inc., USA).
Results: Expression of sFRP-1, sFRP-2, and sFRP-5 in control samples and expression of c-MYC and cyclin D1 in cancer samples showed statistical significance. Significant expression of Wnt3A was observed among patients who had recurrence and were deceased.
Conclusion: Wnt3A, β-catenin, and cyclin D1 are recognized as key components of Wnt/β-catenin signaling. However, in this study, there was no significant expression of all the three genes in OSCC. The proto-oncogene c-MYC showed statistically significant upregulation in cancer tissue samples suggesting that the OSCC among South Indian population is primarily not mediated by the canonical Wnt signaling pathway.

Chen GY, Zheng HC
The clinicopathological and prognostic significances of Dkk3 expression in cancers: A bioinformatics analysis.
Cancer Biomark. 2018; 23(3):323-331 [PubMed] Related Publications
BACKGROUND: Dkk3 protein attenuates the expression of Wnt3a, Wnt5a and LRP6, and their interaction, and interacts with βTrCP to suppress wnt/β-catenin pathway.
METHODS: We performed a bioinformatics analysis of Dkk3 mRNA expression through Oncomine, TCGA and Kaplan-Meier plotter databases up to July 10, 2017.
RESULTS: Up-regulated Dkk3 expression was higher in gastric, breast, and ovarian cancers than normal tissues (p< 0.05). Bitter's database showed a higher Dkk3 expression in ovarian cytoadenocarcinoma than clear cell adenocarcinoma (p< 0.05). Dkk3 was more expressed in ductal breast cancer in situ than invasive ductal breast cancer (p< 0.05), in mixed lobular and ductal cancer, and lobular cancer than ductal breast cancer (p< 0.05). In TCGA data, Dkk3 expression was lower in gastric cancers with than without Barret's esophagus (p< 0.05), in intestinal-type than diffuse-type cancers (p< 0.05), and in the cancers of elder than younger patients (p< 0.05). Dkk3 expression was higher in squamous cell carcinoma than adenocarcinoma (p< 0.05). Dkk3 expression was higher in ductal than lobular breast cancer, or in younger than elder patients with breast cancer (p< 0.05). According to Kaplan-Meier plotter, Dkk3 expression was negatively correlated with overall, progression-free, relapse-free or distant-metastasis-free survival rate of gastric, breast or ovarian cancer patients, but versa for lung cancer patients (p< 0.05).
CONCLUSION: Dkk3 expression might be employed as a potential marker to indicate carcinogenesis and histogenesis, even prognosis.

Guo Z, Liu Z, Yue H, Wang J
Beta-elemene increases chemosensitivity to 5-fluorouracil through down-regulating microRNA-191 expression in colorectal carcinoma cells.
J Cell Biochem. 2018; 119(8):7032-7039 [PubMed] Related Publications
Colorectal carcinoma is a common malignant tumor occurring in the alimentary system. Despite developments of modern medicine, developed resistance to 5-fluorouracil (5-FU) may lead to poor prognosis. Herein, we aimed to explore the effects of beta-elemene on colorectal carcinoma cells (HCT116 and HT29) as well as the underlying mechanisms. Beta-elemene reduced cell viability and induced apoptosis in HCT116 and HT29 cells. Increased apoptosis following beta-elemene exposure was due to enhanced sensitivity to 5-FU through down-regulating miR-191. Expression of key kinases, including Wnt3a, and β-catenin, were down-regulated by beta-elemene through a miR-191 mechanism. Moreover, beta-elemene might improve resistance of colorectal carcinoma cells to 5-FU by down-regulating miR-191, thereby inhibiting the Wnt/β-catenin pathway.

Lee HJ, Li J, Vickman RE, et al.
Cholesterol Esterification Inhibition Suppresses Prostate Cancer Metastasis by Impairing the Wnt/β-catenin Pathway.
Mol Cancer Res. 2018; 16(6):974-985 [PubMed] Article available free on PMC after 01/03/2020 Related Publications
Dysregulation of cholesterol is a common characteristic of human cancers including prostate cancer. This study observed an aberrant accumulation of cholesteryl ester in metastatic lesions using Raman spectroscopic analysis of lipid droplets in human prostate cancer patient tissues. Inhibition of cholesterol esterification in prostate cancer cells significantly suppresses the development and growth of metastatic cancer lesions in both orthotopic and intracardiac injection mouse models. Gene expression profiling reveals that cholesteryl ester depletion suppresses the metastatic potential through upregulation of multiple regulators that negatively impact metastasis. In addition, Wnt/β-catenin, a vital pathway for metastasis, is downregulated upon cholesteryl ester depletion. Mechanistically, inhibition of cholesterol esterification significantly blocks secretion of Wnt3a through reduction of monounsaturated fatty acid levels, which limits Wnt3a acylation. These results collectively validate cholesterol esterification as a novel metabolic target for treating metastatic prostate cancer.

Szemes M, Greenhough A, Melegh Z, et al.
Wnt Signalling Drives Context-Dependent Differentiation or Proliferation in Neuroblastoma.
Neoplasia. 2018; 20(4):335-350 [PubMed] Article available free on PMC after 01/03/2020 Related Publications
Neuroblastoma is one of the commonest and deadliest solid tumours of childhood, and is thought to result from disrupted differentiation of the developing sympathoadrenergic lineage of the neural crest. Neuroblastoma exhibits intra- and intertumoural heterogeneity, with high risk tumours characterised by poor differentiation, which can be attributable to MYCN-mediated repression of genes involved in neuronal differentiation. MYCN is known to co-operate with oncogenic signalling pathways such as Alk, Akt and MEK/ERK signalling, and, together with c-MYC has been shown to be activated by Wnt signalling in various tissues. However, our previous work demonstrated that Wnt3a/Rspo2 treatment of some neuroblastoma cell lines can, paradoxically, decrease c-MYC and MYCN proteins. This prompted us to define the neuroblastoma-specific Wnt3a/Rspo2-driven transcriptome using RNA sequencing, and characterise the accompanying changes in cell biology. Here we report the identification of ninety Wnt target genes, and show that Wnt signalling is upstream of numerous transcription factors and signalling pathways in neuroblastoma. Using live-cell imaging, we show that Wnt signalling can drive differentiation of SK-N-BE(2)-C and SH-SY5Y cell-lines, but, conversely, proliferation of SK-N-AS cells. We show that cell-lines that differentiate show induction of pro-differentiation BMP4 and EPAS1 proteins, which is not apparent in the SK-N-AS cells. In contrast, SK-N-AS cells show increased CCND1, phosphorylated RB and E2F1 in response to Wnt3a/Rspo2, consistent with their proliferative response, and these proteins are not increased in differentiating lines. By meta-analysis of the expression of our 90 genes in primary tumour gene expression databases, we demonstrate discrete expression patterns of our Wnt genes in patient cohorts with different prognosis. Furthermore our analysis reveals interconnectivity within subsets of our Wnt genes, with one subset comprised of novel putative drivers of neuronal differentiation repressed by MYCN. Assessment of β-catenin immunohistochemistry shows high levels of β-catenin in tumours with better differentiation, further supporting a role for canonical Wnt signalling in neuroblastoma differentiation.

Hu J, Guo X, Yang L
Morin inhibits proliferation and self-renewal of CD133
J Pharmacol Sci. 2018; 136(3):114-120 [PubMed] Related Publications
Melanoma is one of the most malignant skin tumors with high mortality rate. Morin has been reported to treat several cancers. However, whether or how Morin affects melanoma progression is still poorly understood. Either Morin treatment or miR-216a overexpression reduced cell viability, sphere formation ability and expressions of stem cell marker genes CD20, CD44, CD133 and Wnt-3A. MiR-216a was induced by Morin treatment in CD133

Sinnberg T, Levesque MP, Krochmann J, et al.
Wnt-signaling enhances neural crest migration of melanoma cells and induces an invasive phenotype.
Mol Cancer. 2018; 17(1):59 [PubMed] Article available free on PMC after 01/03/2020 Related Publications
BACKGROUND: During embryonic development Wnt family members and bone morphogenetic proteins (BMPs) cooperatively induce epithelial-mesenchymal transition (EMT) in the neural crest. Wnt and BMPs are reactivated during malignant transformation in melanoma. We previously demonstrated that the BMP-antagonist noggin blocked the EMT phenotype of melanoma cells in the neural crest and malignant invasion of melanoma cells in the chick embryo; vice-versa, malignant invasion was induced in human melanocytes in vivo by pre-treatment with BMP-2.
RESULTS: Although there are conflicting results in the literature about the role of β-catenin for invasion of melanoma cells, we found Wnt/β-catenin signaling to be analogously important for the EMT-like phenotype of human metastatic melanoma cells in the neural crest and during invasion: β-catenin was frequently expressed at the invasive front of human primary melanomas and Wnt3a expression was inversely correlated with survival of melanoma patients. Accordingly, cytoplasmic β-catenin levels were increased during invasion of melanoma cells in the rhombencephalon of the chick embryo. Fibroblast derived Wnt3a reduced melanoma cell adhesion and enhanced migration, while the β-catenin inhibitor PKF115-584 increased adhesion and reduced migration in vitro and in the chick embryonic neural crest environment in vivo. Similarly, knockdown of β-catenin impaired intradermal melanoma cell invasion and PKF115-584 efficiently reduced liver metastasis in a chick chorioallantoic membrane model. Our observations were accompanied by specific alterations in gene expression which are linked to overall survival of melanoma patients.
CONCLUSION: We present a novel role for Wnt-signaling in neural crest like melanoma cell invasion and metastasis, stressing the crucial role of embryonic EMT-inducing neural crest signaling for the spreading of malignant melanoma.

Wang J, Wang X, Liu F, Fu Y
microRNA-335 inhibits colorectal cancer HCT116 cells growth and epithelial-mesenchymal transition (EMT) process by targeting Twist1.
Pharmazie. 2017; 72(8):475-481 [PubMed] Related Publications
Colorectal cancer is one of the most commonly diagnosed cancers. Recently, several microRNAs (miRNAs) have been characterized as oncogenes or tumor suppressors in colorectal cancer. This study was aimed to explore the tumor suppressive effects and its underling mechanism of miR-335 on colorectal cancer cells. Human colorectal cancer HCT116 cells were employed and the expression of miR-335 in cells was altered by transfection with miR-335 mimic and miR-335 inhibitor. Thereafter, CCK-8 assay, flow cytometry, Transwell assay and Western blotting were used to detect cell viability, apoptosis, migration, invasion, and the expression of epithelial-mesenchymal transition (EMT)-related proteins. Dual luciferase activity assay was performed to test whether Twist1 was a direct target of miR-335. Moreover, cells were co-transfected with miR-335 inhibitor and Twist1 siRNA, and then cell growth and metastasis were re-evaluated. miR-335 overexpression inhibited cell viability, migration and invasion, and promoted apoptotic cells rate. miR-335 overexpression up-regulated E-Cadherin, while down-regulated N-Cadherin, Vimentin and Snail. Twist1 was a direct target of miR-335, and Twist1 silence promoted apoptosis, and abolished miR-335 suppression induced increases in cell viability, migration, invasion, and abnormal expressions of EMT-related proteins. Besides, Twist1 silence abolished miR-335 suppression induced activations of p65 and IκBα, and miR-335 suppression induced up-regulations of Wnt3a, Wnt5a and β-Catenin. miR-335 inhibited HCT116 cells growth, migration, invasion, and ETM process. miR-335 exhibited tumor suppressive effects possibly by inhibition of Twsit1 and thus inactivating NF-κB and Wnt/β-catenin pathways.

Hawkins AG, Basrur V, da Veiga Leprevost F, et al.
The Ewing Sarcoma Secretome and Its Response to Activation of Wnt/beta-catenin Signaling.
Mol Cell Proteomics. 2018; 17(5):901-912 [PubMed] Article available free on PMC after 01/03/2020 Related Publications
Tumor: tumor microenvironment (TME) interactions are critical for tumor progression and the composition and structure of the local extracellular matrix (ECM) are key determinants of tumor metastasis. We recently reported that activation of Wnt/beta-catenin signaling in Ewing sarcoma cells induces widespread transcriptional changes that are associated with acquisition of a metastatic tumor phenotype. Significantly, ECM protein-encoding genes were found to be enriched among Wnt/beta-catenin induced transcripts, leading us to hypothesize that activation of canonical Wnt signaling might induce changes in the Ewing sarcoma secretome. To address this hypothesis, conditioned media from Ewing sarcoma cell lines cultured in the presence or absence of Wnt3a was collected for proteomic analysis. Label-free mass spectrometry was used to identify and quantify differentially secreted proteins. We then used in silico databases to identify only proteins annotated as secreted. Comparison of the secretomes of two Ewing sarcoma cell lines revealed numerous shared proteins, as well as a degree of heterogeneity, in both basal and Wnt-stimulated conditions. Gene set enrichment analysis of secreted proteins revealed that Wnt stimulation reproducibly resulted in increased secretion of proteins involved in ECM organization, ECM receptor interactions, and collagen formation. In particular, Wnt-stimulated Ewing sarcoma cells up-regulated secretion of structural collagens, as well as matricellular proteins, such as the metastasis-associated protein, tenascin C (TNC). Interrogation of published databases confirmed reproducible correlations between Wnt/beta-catenin activation and

Chen Y, Shang H, Zhang S, Zhang X
Ginsenoside Rh2 inhibits proliferation and migration of medulloblastoma Daoy by down-regulation of microRNA-31.
J Cell Biochem. 2018; 119(8):6527-6534 [PubMed] Related Publications
This study aimed to investigate the effects of ginsenoside Rh2 on proliferation, apoptosis, and migration of the human medulloblastoma cell line Daoy, as well as to explore the potential mechanisms of the effects. The human medulloblastoma cell line Daoy was cultured in vitro and treated with or without ginsenoside Rh2. CCK-8 assay was performed to investigate the effect of Rh2 on cell survival using a cell counting Kit-8. Cell proliferation was assessed by BrdU assay. Cell apoptosis was determined using flow cytometry analysis. Cell migration was detected using a modified two-chamber migration assay. MiR-31 mimic and the NC control were transfected into Daoy cells and detected by qRT-PCR. The expression of Wnt3a, Wnt5a, and β-catein was detected by Western blot analysis. Rh2 efficiently suppressed the proliferation and migration, and promoted the apoptosis of Daoy cells. Additionally, Rh2 could down-regulate miR-31. miR-31 overexpression reversed the effects of Rh2 on proliferation, apoptosis and migration of Daoy cells, and activated the Wnt/β-catein signaling pathways in Daoy cells. Rh2 could inhibit the proliferation and migration, and induce apoptosis of Daoy medulloblastoma cells through down-regulation of miR-31 to inactivate the Wnt/β-catein signaling pathway. Therefore, Rh2 may have a utility in clinical applications for the treatment of medulloblastoma.

Kwack MH, Yang JM, Won GH, et al.
Establishment and characterization of five immortalized human scalp dermal papilla cell lines.
Biochem Biophys Res Commun. 2018; 496(2):346-351 [PubMed] Related Publications
Dermal papilla (DP) regulates the growth and cycling of hair follicles. Cultured DP cells are useful for the study of their role in relation to hair growth and regeneration. However, cultivation of human DP cells is tedious and difficult. In addition, cultured DP cells possess a relatively short replicative life span, requiring immortalized human DP cell lines. We previously established an immortalized human DP cell line, SV40T-hTERT-DPC, by introducing human telomerase reverse transcriptase (hTERT) gene into the transformed cell line, SV40T-DPC. In this study, we co-transfected the simian virus 40 large T antigen (SV40T-Ag) and hTERT into DP cells from scalp hair follicles from a male with androgenetic alopecia and established five immortalized DP cell lines and named KNU-101, KNU-102, KNU-103, KNU-201 and KNU-202. We then evaluated tumorigenicity, expression of DP markers, responses to androgen, Wnt3a and BMP4, and expression of DP signature genes. These cell lines displayed early passage morphology and maintained responses to androgen, Wnt and BMP. Furthermore, these cell lines expressed DP markers and DP signature genes. KNU cell lines established in this study are potentially useful sources for hair research.

Wang ZM, Wan XH, Sang GY, et al.
miR-15a-5p suppresses endometrial cancer cell growth via Wnt/β-catenin signaling pathway by inhibiting WNT3A.
Eur Rev Med Pharmacol Sci. 2017; 21(21):4810-4818 [PubMed] Related Publications
OBJECTIVE: Endometrial cancer is one of the three most common types of gynecologic cancer. The global incidence has increased in recent years. microRNAs (miRNAs) regulate numerous biological processes by binding to the 3'UTR of target mRNA to down-regulate protein synthesis.
PATIENTS AND METHODS: Endometrial cancer patients received surgeries in our hospital were enrolled. MiR-15a-5p mimic or miR-15a-5p inhibitor was transfected into HEC-1-A cells by lentivirus. Colony formation assay was applied for detecting cell proliferation. Real-time PCR was performed to test miRNA and mRNA expression. Western blot was used to detect protein level. ChIP was adopted to test transcription activation. TOP/FOP was tested to determine Wnt signaling pathway activity. A dual-luciferase reporter assay was used to confirm miRNA target.
RESULTS: miR-15a-5p was decreased in endometrial cancer cells and tissues. miR-15a-5p overexpression restrained HEC-1-A cell proliferation and stemness. miR-15a-5p mimic transfection reduced mRNA and protein levels of the proteins which are related to cell proliferation and Wnt signaling pathway. MiR-15a-5p targeted a putative binding site in the 3'-UTR of Wnt3a gene, thus regulating Wnt signaling pathway. miR-15a-5p overexpression decreased Wnt3a protein expression. Wnt3a presented significant negative correlation with the miR-15a-5p level in endometrial cancer patients.
CONCLUSIONS: miR-15a-5p is a regulator of endometrial cancer cell proliferation by directly targeting Wnt3a to block Wnt signaling pathway.

Ivonne Wence-Chavez L, Palomares-Chacon U, Pablo Flores-Gutierrez J, et al.
Gene expression profiling demonstrates WNT/β-catenin pathway genes alteration in Mexican patients with colorectal cancer and diabetes mellitus.
J BUON. 2017 Sep-Oct; 22(5):1107-1114 [PubMed] Related Publications
PURPOSE: Several studies have shown a strong association between diabetes mellitus (DM) and increased risk of colorectal cancer (CRC). The fundamental mechanisms that support this association are not entirely understood; however, it is believed that hyperinsulinemia and hyperglycemia may be involved. Some proposed mechanisms include upregulation of mitogenic signaling pathways like MAPK, PI3K, mTOR, and WNT, which are involved in cell proliferation, growth, and cancer cell survival. The purpose of this study was to evaluate the gene expression profile and identify differently expressed genes involved in mitogenic pathways in CRC patients with and without DM.
METHODS: In this study, microarray analysis of gene expression followed by quantitative PCR (qPCR) was performed in cancer tissue from CRC patients with and without DM to identify the gene expression profiles and validate the differently expressed genes.
RESULTS: Among the study groups, some differently expressed genes were identified. However, when bioinformatics clustering tools were used, a significant modulation of genes involved in the WNT pathway was evident. Therefore, we focused on genes participating in this pathway, such as WNT3A, LRP6, TCF7L2, and FRA-1. Validation of the expression levels of those genes by qPCR showed that CRC patients without type 2 diabetes mellitus (T2DM) expressed significantly more WNT3Ay LRP6, but less TCF7L2 and FRA-1 compared to controls, while in CRC patients with DM the expression levels of WNT3A, LRP6, TCF7L2, and FRA-1 were significantly higher compared to controls.
CONCLUSIONS: Our results suggest that WNT/β-catenin pathway is upregulated in patients with CRC and DM, demonstrating its importance and involvement in both pathologies.

Chakraborty C, Samadder S, Roychowdhury A, et al.
Activation of Wnt-β-catenin pathway in basal-parabasal layers of normal cervical epithelium comparable during development of uterine cervical carcinoma.
Mol Cell Biochem. 2018; 443(1-2):121-130 [PubMed] Related Publications
In this study, importance of Wnt-β-catenin pathway in the development of uterine cervical carcinoma was evaluated. For this purpose, the profiles (expression/methylation/deletion) of β-catenin, p-β-catenin (Y654), Wnt3a, and APC were studied in disease free normal cervical epithelium (n = 9), adjacent normal cervical epithelium of primary tumors (n = 70), CIN (n = 28), CACX (n = 102) samples, and two CACX cell lines (HeLa and SiHa). Immunohistochemical analysis revealed high/medium (74-95%) expression of β-catenin/p-β-catenin (Y654) and Wnt3a and low expression (23-26%) of APC in proliferating basal-parabasal layers contrary to differentiated spinous layer in normal cervix irrespective of HPV16 infection. The expression profile of the genes in the basal-parabasal layers did not change significantly during development of CACX. High (66%) promoter methylation of APC was seen in basal-parabasal layers and the cervical lesions (42-69%), unlike in spinous layers (25%). The promoter methylation status of APC was validated by in vitro demethylation experiments using 5-aza-dC in CACX cell lines. However, additional deletion of APC was significantly increased from CIN (12%) to stage I/II (40%) and became comparable in stage III/IV (48%) of the tumor. Patients with alterations (deletion/methylation) of APC and high/medium expression of Wnt3a/β-catenin/p-β-catenin (Y654) showed significantly poor survival. Thus our data indicate that cumulative effect of Wnt3a overexpression and APC inactivation are needed for overexpression of β-catenin during the development of CACX.

Disclaimer: This site is for educational purposes only; it can not be used in diagnosis or treatment.

Cite this page: Cotterill SJ. WNT3A, Cancer Genetics Web: http://www.cancer-genetics.org/WNT3A.htm Accessed:

Creative Commons License
This page in Cancer Genetics Web by Simon Cotterill is licensed under a Creative Commons Attribution-ShareAlike 4.0 International License.
Note: content of abstracts copyright of respective publishers - seek permission where appropriate.

 [Home]    Page last revised: 01 September, 2019     Cancer Genetics Web, Established 1999