Gene Summary

Gene:CD82; CD82 molecule
Aliases: R2, 4F9, C33, IA4, ST6, GR15, KAI1, SAR2, TSPAN27
Summary:This metastasis suppressor gene product is a membrane glycoprotein that is a member of the transmembrane 4 superfamily. Expression of this gene has been shown to be downregulated in tumor progression of human cancers and can be activated by p53 through a consensus binding sequence in the promoter. Its expression and that of p53 are strongly correlated, and the loss of expression of these two proteins is associated with poor survival for prostate cancer patients. Two alternatively spliced transcript variants encoding distinct isoforms have been found for this gene. [provided by RefSeq, Jul 2008]
Databases:OMIM, VEGA, HGNC, Ensembl, GeneCard, Gene
Protein:CD82 antigen
Source:NCBIAccessed: 27 February, 2015


What does this gene/protein do?
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Cancer Overview

Research Indicators

Publications Per Year (1990-2015)
Graph generated 27 February 2015 using data from PubMed using criteria.

Literature Analysis

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Tag cloud generated 27 February, 2015 using data from PubMed, MeSH and CancerIndex

Specific Cancers (8)

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: CD82 (cancer-related)

Marino N, Collins JW, Shen C, et al.
Identification and validation of genes with expression patterns inverse to multiple metastasis suppressor genes in breast cancer cell lines.
Clin Exp Metastasis. 2014; 31(7):771-86 [PubMed] Related Publications
Metastasis suppressor genes (MSGs) have contributed to an understanding of regulatory pathways unique to the lethal metastatic process. When re-expressed in experimental models, MSGs block cancer spread to, and colonization of distant sites without affecting primary tumor formation. Genes have been identified with expression patterns inverse to a single MSG, and found to encode functional, druggable signaling pathways. We now hypothesize that common signaling pathways mediate the effects of multiple MSGs. By gene expression profiling of human MCF7 breast carcinoma cells expressing a scrambled siRNA, or siRNAs to each of 19 validated MSGs (NME1, BRMS1, CD82, CDH1, CDH2, CDH11, CASP8, MAP2K4, MAP2K6, MAP2K7, MAPK14, GSN, ARHGDIB, AKAP12, DRG1, CD44, PEBP1, RRM1, KISS1), we identified genes whose expression was significantly opposite to at least five MSGs. Five genes were selected for further analysis: PDE5A, UGT1A, IL11RA, DNM3 and OAS1. After stable downregulation of each candidate gene in the aggressive human breast cancer cell line MDA-MB-231T, in vitro motility was significantly inhibited. Two stable clones downregulating PDE5A (phosphodiesterase 5A), an enzyme involved in the regulation of cGMP-specific signaling, exhibited no difference in cell proliferation, but reduced motility by 47 and 66 % compared to the empty vector-expressing cells (p = 0.01 and p = 0.005). In an experimental metastasis assay, two shPDE5A-MDA-MB-231T clones produced 47-62 % fewer lung metastases than shRNA-scramble expressing cells (p = 0.045 and p = 0.009 respectively). This study demonstrates that previously unrecognized genes are inversely related to the expression of multiple MSGs, contribute to aspects of metastasis, and may stand as novel therapeutic targets.

Wu J, Liang S, Bergholz J, et al.
ΔNp63α activates CD82 metastasis suppressor to inhibit cancer cell invasion.
Cell Death Dis. 2014; 5:e1280 [PubMed] Related Publications
P63 is a p53 family member involved in multiple facets of biology, including embryonic development, cell proliferation, differentiation, survival, apoptosis, senescence and aging. The p63 gene encodes multiple protein isoforms either with (TAp63) or without (ΔNp63) the N-terminal transactivation domain. Amounting evidence suggests that p63 can function as a tumor suppressor, yet the precise molecular mechanisms, and particularly the specific roles of TAp63 and ΔNp63 in cancer progression, are still largely unclear. Here, we demonstrated that ΔNp63α, the predominant isoform expressed in epithelial cells and squamous cell carcinomas, inhibits cell invasion. Affymetrix gene expression profiling, combined with gain- and loss-of-function analyses and chromatin immunoprecipitation, indicated that cluster of differentiation 82 (CD82), a documented metastasis suppressor, is a direct transcriptional target of ΔNp63α. Expression of ΔNp63α inhibited outgrowth in Matrigel and cancer cell invasion, which was largely reversed by specific ablation of CD82. Conversely, ΔNp63α knockdown led to increased cell invasion, which was reversed by ectopic expression of CD82. Moreover, inhibition of glycogen synthase kinase-3β (GSK3β) by either pharmacological inhibitors or by RNA interference resulted in the downregulation of ΔNp63α and CD82 expression, concomitant with increased cell invasion, independently of β-catenin. Furthermore, decreased expression of p63 and CD82 is correlated with cancer progression. Taken together, this study reveals that ΔNp63α upregulates CD82 to inhibit cell invasion, and suggests that GSK3β can regulate cell invasion by modulating the ΔNp63α-CD82 axis.

Yu L, Zhou L, Wu S, et al.
Clinicopathological significance of cancer stem cells marked by CD133 and KAI1/CD82 expression in laryngeal squamous cell carcinoma.
World J Surg Oncol. 2014; 12:118 [PubMed] Free Access to Full Article Related Publications
BACKGROUND: Presently, CD133 is one of the hottest markers to characterize cancer stem cells and KAI1/CD82 is reported as an important marker for the metastasis and prognosis of many cancers. The purpose of our study is to explore the relationship between cancer stem cells (CSCs) marked by CD133 and KAI1/CD82 expression and the clinicopathological characteristics of patients with laryngeal squamous cell carcinoma (LSCC).
METHODS: Immunohistochemical analysis was used to detect the expression of CD133 and KAI1/CD82 in 83 archival surgical specimens of human LSCC and 83 cases of normal laryngeal tissues.
RESULTS: In LSCC, positive rates of 49.4% and 41.0% were obtained for CD133 and KAI1/CD82, respectively. The expression of CD133 in LSCC tissues was significantly higher than that in normal tissues (P<0.001), and the expression of CD133 was positively associated with pTNM stage (P=0.005), pathological grade (P=0.001), and lymph node metastasis (P<0.001). The reduced expression of KAI1/CD82 was present in LSCC tissues. The positive rate of KAI1/CD82 expression was negatively correlated with pTNM stage (P=0.014), pathological grade (P<0.001), and lymph node metastasis (P=0.007). A correlation analysis showed that there was a negative relationship between the expression of CD133 and KAI1/CD82 protein in LSCC tissues (P<0.001). By Kaplan-Meier analysis, the expression of CD133 was negatively correlated with overall survival (OS) (log-rank=40.949, P<0.001) and disease-free survival (DFS) (log-rank=39.307, P<0.001) time of LSCC. The expression of KAI1/CD82 was positively correlated with OS (log-rank=40.279, P<0.001) and DFS (log-rank=39.271, P<0.001) time of LSCC. Cox regression analysis: the expression of CD133 and KAI1/CD82, and pTNM stages were independent prognostic factors of LSCC (P<0.05).
CONCLUSIONS: Thus the detection of CD133 and KAI1/CD82 proteins may be used as a potential indicator of LSCC prognosis.

Ding C, Cheng S, Yang Z, et al.
Long non-coding RNA HOTAIR promotes cell migration and invasion via down-regulation of RNA binding motif protein 38 in hepatocellular carcinoma cells.
Int J Mol Sci. 2014; 15(3):4060-76 [PubMed] Free Access to Full Article Related Publications
Long non-coding RNA HOTAIR exerts regulatory functions in various biological processes in cancer cells, such as proliferation, apoptosis, mobility, and invasion. We previously found that HOX transcript antisense RNA (HOTAIR) is a negative prognostic factor and exhibits oncogenic activity in hepatocellular carcinoma (HCC). In this study, we aimed to investigate the role and molecular mechanism of HOTAIR in promoting HCC cell migration and invasion. Firstly, we profiled its gene expression pattern by microarray analysis of HOTAIR loss in Bel-7402 HCC cell line. The results showed that 129 genes were significantly down-regulated, while 167 genes were significantly up-regulated (fold change >2, p < 0.05). Bioinformatics analysis indicated that RNA binding proteins were involved in this biological process. HOTAIR suppression using RNAi strategy with HepG2 and Bel-7402 cells increased the mRNA and protein expression levels of RNA binding motif protein 38 (RBM38). Moreover, the expression levels of RBM38 in HCC specimens were significantly lower than paired adjacent noncancerous tissues. In addition, knockdown of HOTAIR resulted in a decrease of cell migration and invasion, which could be specifically rescued by down-regulation of RBM38. Taken together, HOTAIR could promote migration and invasion of HCC cells by inhibiting RBM38, which indicated critical roles of HOTAIR and RBM38 in HCC progression.

Dai W, Wang C, Wang F, et al.
Anti-miR-197 inhibits migration in HCC cells by targeting KAI 1/CD82.
Biochem Biophys Res Commun. 2014; 446(2):541-8 [PubMed] Related Publications
AIM: To investigate the metastatic effects and mechanisms of miR-197 in hepatocellular carcinoma (HCC).
METHODS AND RESULTS: The levels of miR-197 increased in HCC cells and tissues compared with a normal hepatic cell line (LO2) and adjacent nontumorous liver tissues, respectively. miR-197 expression negatively correlated with CD82 mRNA expression in these cell lines and tissues. Dual luciferase reporter assay and Western blot confirmed a direct interaction between miR-197 and CD82 3'UTR sequences. After miR-197 was silenced in HCC cells, CD82 expression increased. In the presence of human hepatocyte growth factor (HGF), cells silenced for anti-miR-197 exhibited elongated cellular tails and diminished lamellipodia due to reductions in both ROCK activity and the levels of Rac 1 protein. Downregulation of miR-197 along with the upregulation of CD82 in HCC cells resulted in the inhibition of HCC migration and invasion in vitro and in vivo.
CONCLUSION: Taken together, these data suggest that anti-miR-197 suppresses HCC migration and invasion by targeting CD82. The regulation of the miR-197/CD82 axis could be a novel therapeutic target in future HCC effective therapy.

Kwon HJ, Min SY, Park MJ, et al.
Expression of CD9 and CD82 in clear cell renal cell carcinoma and its clinical significance.
Pathol Res Pract. 2014; 210(5):285-90 [PubMed] Related Publications
CD9 and CD82, members of the tetraspanin family, act as metastasis suppressors in many human malignant tumors, but the role of these molecules is not well known in clear cell renal cell carcinoma (CCRCC). This study was designed to evaluate the immunohistochemical expression of CD9 and CD82 in 644 cases of CCRCC and to determine the clinicopathologic and prognostic significance of their expression. The percentage of positive tumor cells was evaluated, and the expression was classified into 2 categories: low expression (less than 10% positive cells) or high expression (more than 10% positive cells) for CD9 expression and negative (no positive cells) or positive for CD82 expression. CD9 high expression was found in 303 (47.0%) patients, and CD82 positivity was found in 98 (15.2%) patients. High expression of CD9 was statistically associated with older patients (p=0.003). The cases showing positive immunoreactivity for CD82 exhibited a high stage (p<0.001) and high nuclear grade (p<0.001). The overall, cancer-specific and progression-free survival rates were significantly higher in patients with a CD82-negative profile compared to patients with a CD82-positive profile (p<0.001). Although the biological function of CD82 in CCRCC remains unclear, the CCRCC patients with CD82 positive expression show poor prognosis.

Liu X, Guo XZ, Li HY, et al.
KAI1 inhibits lymphangiogenesis and lymphatic metastasis of pancreatic cancer in vivo.
Hepatobiliary Pancreat Dis Int. 2014; 13(1):87-92 [PubMed] Related Publications
BACKGROUND: Several studies have shown that KAI1 inhibits tumor metastasis, but its mechanism is not clear. The present study aimed to determine the role of KAI1 in lymphatic metastasis, specifically in pancreatic cancer.
METHODS: The KAI1 gene was transfected into the pancreatic cancer cell line MIA PaCa-2 and PANC-1 by using liposomes and selected by G418, and the protein was measured by Western blotting. After successful infection, the cell growth curve was studied by MTT, vascular endothelial growth factor C (VEGF-C) secretion by pancreatic cancer cell were measured by ELISA. The KAI1 and pCMV transfected MIA PaCa-2 cells were renamed as MIA PaCa-2-K and MIA PaCa-2-p. These two kinds of cells were injected into the subcuticular layer of nude mice; both tumor growth and metastasis through the lymphatic nodes were assessed. Lymphangiogenesis in tumors was measured by immunohistochemistry.
RESULTS: The VEGF-C secretion was significantly reduced in MIA PaCa-2 cells compared with PANC-1 cells after being transfected with the KAI1 gene. The growth rate of subcutaneous tumors was similar after the injection of MIA PaCa-2-K, MIA PaCa-2, and MIA PaCa-2-p. MIA PaCa-2-K tumors showed slower lymphangiogenesis and lymph node metastasis compared with MIA PaCa-2 and MIA PaCa-2-p tumors.
CONCLUSION: The overexpression of KAI1 inhibits the lymphangiogenesis and lymph node metastasis of MIA PaCa-2 pancreatic tumors.

Nankivell P, Williams H, McConkey C, et al.
Tetraspanins CD9 and CD151, epidermal growth factor receptor and cyclooxygenase-2 expression predict malignant progression in oral epithelial dysplasia.
Br J Cancer. 2013; 109(11):2864-74 [PubMed] Free Access to Full Article Related Publications
BACKGROUND: Prognostic biomarkers aim to improve on the current inadequate method of histological assessment to identify patients with oral epithelial dysplasia at greatest risk of malignant transformation. We aimed to assess the prognostic ability of six protein biomarkers linked to the epidermal growth factor receptor (EGFR) pathway, including three tetraspanins, in a large multicentre oral dysplasia cohort.
METHODS: One hundred and forty-eight cases with varying degrees of epithelial dysplasia underwent immunohistochemical assessment for CD9, CD151, CD82, EGFR, Her-2, and COX-2. Scoring was performed independently by two observers. Univariate analyses using both logistic and Cox regression models and a multivariate regression were performed.
RESULTS: Malignant progression was significantly greater in those cases with decreased expression of CD9 (P=0.02), and increased expression of CD151 (P=0.02), EGFR (P=0.04), and COX-2 (P=0.003). Histological grade (P=0.0002) and morphology (P=0.03) were also prognostic, whereas smoking and alcohol were not. The optimal combination by backward-variable selection was of histological grade (hazard ratio (HR) 1.64; 95% CI 1.12, 2.40), COX-2 overexpression (HR 1.12; 1.02, 1.24) and CD9 underexpression (HR 0.88; 0.80, 0.97). CD82 and Her-2 demonstrated no prognostic ability.
CONCLUSION: This is the first study of the expression and prognostic potential of the tetraspanins in oral dysplasia. A combination of certain biomarkers with clinical factors appeared to improve the accuracy of determining the risk of malignancy in individuals with oral dysplasia. These findings may also offer potential new therapeutic approaches for this condition.

Tang Y, Cheng Y, Martinka M, et al.
Prognostic significance of KAI1/CD82 in human melanoma and its role in cell migration and invasion through the regulation of ING4.
Carcinogenesis. 2014; 35(1):86-95 [PubMed] Related Publications
KAI1/CD82 is a member of the transmembrane 4 superfamily, which was first identified as a metastasis suppressor for prostate cancer. The expression of KAI1 was found to be reduced in many types of cancers, including prostate, breast, ovarian, cervical and endometrial cancer. However, the role of KAI1 in melanoma pathogenesis is not known. In this study, we investigated the expression level of KAI1 in a large set of melanocytic lesions at different stages. We found that the expression of KAI1 is significantly decreased during melanoma progression. In fact, KAI1 expression is drastically reduced in primary melanoma compared with dysplastic nevi (P = 1.8×10(-4)) and further reduced in metastatic melanoma compared with primary melanoma (P = 9.4 × 10(-15)). Furthermore, decreased KAI1 staining is strongly correlated with a worse 5 year and 10 year patient survival. Multivariate Cox regression analysis showed that KAI1 is also an independent prognostic factor for both 5 year and 10 year survival. Moreover, we found that overexpression of KAI1 significantly inhibited melanoma cell migration through suppression of Rho-associated kinase-mediated formation of stress fiber. Our data also suggested that overexpression of KAI1 significantly inhibited melanoma cell invasion by reducing the activity of metalloproteinase-2. In addition, we found that suppression of melanoma cell migration by KAI1 is mediated by another tumor-suppressor protein called inhibitor of growth 4 through the regulation of p65. Taken together, our data suggest that KAI1 may be used as a promising prognostic marker and a possible therapeutic target for human melanoma.

Yu L, Wu S, Zhou L, et al.
[Expressions of CD133 and CD82/KAI1 in bladder urothelial carcinoma and their correlation with vasculogenic mimicry].
Nan Fang Yi Ke Da Xue Xue Bao. 2013; 33(9):1336-40 [PubMed] Related Publications
OBJECTIVE: To explore the expressions of CD133 and CD82/KAI1 in bladder urothelial carcinoma, their association with the clinicopathological factors and their roles in vasculogenic mimicry (VM) in the tumor.
METHODS: The expressions of CD133 and CD82/KAI1 and VM were detected by immunohistochemistry and histochemistry in 90 specimens of bladder urothelial carcinoma and 20 specimens of normal bladder epithelium tissue.
RESULTS: The positivity rates of CD133, CD82/KAI1 and VM in normal bladder epithelium tissue were 0, 90% and 0, showing significant differences from the rates of 65.6%, 31.1% and 31.1% in urothelial carcinoma, respectively (P<0.01). Positive expressions of CD133, CD82/KAI1 and VM were significantly correlated with pTNM stage and tumor relapse (P<0.01) but not with gender, age, or tumor numbers (P>0.05). CD133 expression was positively correlated with VM (P=0.487, P<0.05), and CD82/KAI1 expression was negatively correlated with VM (r=-0.452, P<0.01) and CD133 (r=-0.776, P<0.05).
CONCLUSION: The expressions of CD133 and CD82/KAI1 proteins are involved in the occurrence of VM in bladder urothelial carcinoma to contribute to the invasion and relapse of bladder carcinoma.

Kuroda N, Tanaka A, Ohe C, Nagashima Y
Recent advances of immunohistochemistry for diagnosis of renal tumors.
Pathol Int. 2013; 63(8):381-90 [PubMed] Related Publications
The recent classification of renal tumors has been proposed according to genetic characteristics as well as morphological difference. In this review, we summarize the immunohistochemical characteristics of each entity of renal tumors. Regarding translocation renal cell carcinoma (RCC), TFE3, TFEB and ALK protein expression is crucial in establishing the diagnosis of Xp11.2 RCC, renal carcinoma with t(6;11)(p21;q12), and renal carcinoma with ALK rearrangement, respectively. In dialysis-related RCC, neoplastic cells of acquired cystic disease-associated RCC are positive for alpha-methylacyl-CoA racemase (AMACR), but negative for cytokeratin (CK) 7, whereas clear cell papillary RCC shows the inverse pattern. The diffuse positivity for carbonic anhydrase 9 (CA9) is diagnostic for clear cell RCC. Co-expression of CK7 and CA9 is characteristic of multilocular cystic RCC. CK7 and AMACR are excellent markers for papillary RCC and mucinous tubular and spindle cell carcinoma. CD82 and epithelial-related antigen (MOC31) may be helpful in the distinction between chromophobe RCC and renal oncocytoma. WT1 and CD57 highlights the diagnosis of metanephric adenoma. The combined panel of PAX2 and PAX8 may be useful in the diagnosis of metastatic RCC.

Zhang BH, Liu W, Li L, et al.
KAI1/CD82 and MRP1/CD9 serve as markers of infiltration, metastasis, and prognosis in laryngeal squamous cell carcinomas.
Asian Pac J Cancer Prev. 2013; 14(6):3521-6 [PubMed] Related Publications
OBJECTIVE: The current study explored the expression of KAI1/CD82 and MRP1/CD9 and its significance in laryngeal squamous cell carcinoma (LSCC).
METHODS: The expression levels of KAI1/CD82 and MRP1/CD9 in 100 LSCC tissue specimens, as well as in 30 para-LSCC non-carcinomatous tissue specimens randomly taken from the patients, were assessed using the quantitative polymerase chain reaction (Q-PCR) and immunohistochemistry and correlations with pathological parameters of LSCC and their influence on survival function were analyzed.
RESULTS: KAI1/CD82 and MRP1/CD9 showed basically consistent changes in both mRNA and protein expression. Their expression in the 30 LSCC specimens was significantly lower compared with that in the corresponding non-carcinous tissues (P < 0.01 or 0.05), notably correlating with TNM stage, differentiation degree, clinical stage, and lymphatic metastasis (P < 0.01 or 0.05), but not gender, age, and LSCC growth sites (P > 0.05). The median survival of patients with positive KAI1/CD82 and MRP1/CD9 protein expression was longer than that of patients with negative protein expression (P < 0.01 or 0.05). KAI1/CD82 protein expression negatively correlated with MRP1/CD9 protein expression in LSCC (χ(2) = 31.25, P < 0.01).
CONCLUSION: KAI1/CD82 and MRP1/CD9 may jointly participate in the development of LSCC. They may serve as the markers for judging the infiltration, metastasis, and prognosis of LSCC.

Khanna P, Chung CY, Neves RI, et al.
CD82/KAI expression prevents IL-8-mediated endothelial gap formation in late-stage melanomas.
Oncogene. 2014; 33(22):2898-908 [PubMed] Related Publications
Melanoma cells facilitate endothelial gap formation, the first step during tumor transendothelial migration, which is mediated by both adhesion and endogenously produced chemokines (in particular, interleukin-8 (IL-8)). Tetraspanins are localized to the cell surface in cancer and participate in various functions including invasion of tissues mediated by secretion of cytokines and matrix metalloproteinases. However, little is known about the role of CD82 tetraspanins in malignant melanomas during cancer cell invasion. In this study, we investigated the functional importance of CD82 expression in melanoma-mediated gap formation by using cDNAs to induce CD82 expression in highly invasive melanoma cell lines. Results showed that CD82 expression inhibited melanoma cell-induced gap formation, melanoma cell extravasation in vitro and subsequent lung metastasis development in vivo. Mechanistic studies showed that inducible expression of CD82 in highly metastatic melanoma cells significantly increased p21 expression upon binding of Duffy antigen receptor group (DARC), inducing tumor cell senescence and interrupting IL-8-mediated vascular endothelial (VE)-cadherin disassembly. Taken together, these studies provide a rationale for using drug therapies that restore CD82 expression and inhibit IL-8 production to inhibit late-stage melanoma cell extravasation and subsequent metastasis development.

Ma ZB, Li K, Wang J, Guo GH
Role of KAI1/CD82 polymorphisms in colon cancer risk in Han Chinese population.
Med Oncol. 2013; 30(3):668 [PubMed] Related Publications
The aim of this study is to investigate the associations between KAI1/CD82 gene polymorphisms and colorectal cancer (CRC)-risk predisposition. We undertook a case-control study to analyze two KAI1/CD82 polymorphisms (exon 3 -29166 C>T and exon 9 -52840 C>A) in an Han Chinese population, by extraction of genomic DNA from the peripheral blood of 356 patients with CRC and 378 control participants, and performed KAI1/CD82 genotyping using DNA sequencing. The obtained results indicated that overall, no statistically significant association was observed in exon 9 (-52840 C>A). Nevertheless, exon 3 (-29166 C>T) genotype was at increased risk of CRC (P = 0.006; odds ratio = 1.299, CI 95% 1.058-1.549). Furthermore, -29166 T allele CRCs were more significantly common in patients with tumor size of >4 cm than C allele CRC and in cases of poor differentiation and advanced pathological stage. These findings led us to conclude that polymorphism in exon 3 (-29166 C>T) was observed to be associated with susceptibility of CRC. However, exon 9 (-52840 C>A) polymorphism showed no correlation to CRC susceptibility. Nevertheless, further investigation with a larger sample size is needed to support our results.

Nishioka C, Ikezoe T, Yang J, et al.
CD82 regulates STAT5/IL-10 and supports survival of acute myelogenous leukemia cells.
Int J Cancer. 2014; 134(1):55-64 [PubMed] Related Publications
We recently reported that adhesion molecule CD82 is aberrantly expressed in CD34(+) /CD38(-) leukemia stem cells (LSCs). Here, we report the results of a functional analysis of CD82 in CD34(+) /CD38(-) acute myelogenous leukemia (AML) cells. Short hairpin (sh)RNA-mediated downregulation of CD82 resulted in a decrease in the level of IL-10. In contrast, forced expression of CD82 in CD34(+)/CD38(+) AML cells by transduction with CD82-expressing lentiviral particles resulted in an increase in the levels of IL-10. Notably, exposure of CD34(+)/CD38(-) AML cells to IL-10 stimulated clonogenic growth of these cells. Moreover, downregulation of CD82 by a shRNA dephosphorylated STAT5 in CD34(+)/CD38(-) AML cells. On the other hand, forced expression of CD82 resulted in increase in the levels of p-STAT5 in CD34(+)/CD38(+) AML cells. Chromatin immunoprecipitation (ChIP) assay results indicated that STAT5A binds to the promoter region of the IL-10 gene, while reporter gene assay results indicated stimulation of IL-10 expression at the transcriptional level. These results suggest that CD82 positively regulates the STAT5/IL-10 signaling pathway. Moreover, shRNA-mediated downregulation of CD82 expression in CD34(+)/CD38(-) AML cells dephosphorylated STAT5 in immunodeficient mice. Taken together, our data suggest that the CD82/STAT5/IL-10 signaling pathway is involved in the survival of CD34(+)/CD38(-) AML cells and may thus be a promising therapeutic target for eradication of AML LSCs.

Tsui KH, Wang SW, Chung LC, et al.
Mechanisms by which interleukin-6 attenuates cell invasion and tumorigenesis in human bladder carcinoma cells.
Biomed Res Int. 2013; 2013:791212 [PubMed] Free Access to Full Article Related Publications
Interleukin-6, a multifunctional cytokine, contributes to tumor cell proliferation and differentiation. However, the biological mechanisms that are affected by the expression of interleukin-6 in bladder cancer cells remain unclear. We evaluated the effects of interleukin-6 expression in human bladder carcinoma cells in vitro and in vivo. The results of interleukin-6-knockdown experiments in T24 cells and interleukin-6-overexpression experiments in HT1376 cells revealed that interleukin-6 reduced cell proliferation, migration, and invasion in vitro. Xenograft animal studies indicated that the overexpression of interleukin-6 downregulated tumorigenesis of bladder cells and that interleukin-6 knockdown reversed this effect. The results of RT-PCR, immunoblotting, and reporter assays indicated that the overexpression of interleukin-6 upregulated the expression of the mammary serine protease inhibitor (MASPIN), N-myc downstream gene 1 (NDRG1), and KAI1 proteins in HT1376 cells and that interleukin-6 knockdown reduced the expression of these proteins in T24 cells. In addition, results of immunoblotting assays revealed that interleukin-6 modulated epithelial-mesenchymal transitions by upregulating the expression of the E-cadherin, while downregulation N-cadherin and vimentin proteins. Our results suggest that the effects of interleukin-6 on the regulation of epithelial-mesenchymal transitions and the expressions of the MASPIN, NDRG1, and KAI1 genes attribute to the modulation of tumorigenesis in human bladder carcinoma cells.

Wu SW, Yu L, Zhou L, et al.
[Expression of Gal-3 and CD82/KAI1 proteins in non-small cell lung cancer and their clinical significance].
Zhonghua Zhong Liu Za Zhi. 2013; 35(2):124-8 [PubMed] Related Publications
OBJECTIVE: To study the expression of galectin 3 (Gal-3) and CD82/KAI1 proteins in non-small cell lung cancer (NSCLC) and the correlation between their expression and clinical significance.
METHODS: The expression of Gal-3 and CD82/KAI1 proteins was detected by immunohistochemistry in 160 specimens of NSCLC and 20 specimens of normal lung tissue.
RESULTS: The positive rates of Gal-3 and CD82/KAI1 proteins in the NSCLC were 63.8% and 37.5%, respectively, the positive rates of Gal-3 and CD82/KAI1 proteins in the normal lung tissue were 25.0% and 95.0%, respectively, and there was a significant difference between the two groups (P < 0.01). The expression of Gal-3 and CD82/KAI1 proteins was significantly correlated with the grade of tumor, lymph node metastasis, and pathological-TNM stages (all P < 0.05). Spearman analysis showed that there was a negative correlation between expressions of Gal-3 and CD82/KAI1 in NSCLC (r = -0.732, P < 0.01). Overexpression of Gal-3 and low expression of CD82/KAI1 were related to poor prognosis: the survival rate was significantly lower in the positive Gal-3 group (survival time: 23.0 ± 17.5 months) than that in the negative group (survival time: 71.6 ± 21.6 months) (P < 0.01). The survival rates of the CD82/KAI1-positive group (survival time: 72.5 ± 19.5 months) and CD82/KAI1-negative group (survival time: 21.6 ± 16.1 months) were significantly different (P < 0.01). Multivariate analysis indicated that pTNM stage and positive expression of Gal-3 and CD82/KAI1 are independent prognostic factors of NSCLC (P < 0.01).
CONCLUSIONS: The expression of Gal-3 and CD82/KAI1 may be related to the initiation, development and metastasis of NSCLC. Combined detection of Gal-3 and CD82/KAI1 has an important role in predicting the progression and prognosis of NSCLC.

Zhang B, Liu W, Li L, et al.
KAI1/CD82 and cyclin D1 as biomarkers of invasion, metastasis and prognosis of laryngeal squamous cell carcinoma.
Int J Clin Exp Pathol. 2013; 6(6):1060-7 [PubMed] Free Access to Full Article Related Publications
OBJECTIVE: This study aimed to investigate the expressions and significance of KAI1/CD82 and cyclin D1 in laryngeal squamous cell carcinoma (LSCC).
METHODS: Real-time quantitative PCR (Q-PCR) and Western blot assay were employed to detect the expressions of KAI1/CD82 and cyclin D1 in the laryngeal tissues of 86 LSCC patients, 32 patients with laryngeal polyp and 38 patients with laryngeal leukoplakia, and the influence of both proteins on the clinicopathological features and survival of LSCC patients.
RESULTS: The changes in mRNA and protein expressions of KAI1/CD82 and cyclin D1 were consistent in three groups, and the expressions of KAI1/CD82 and cyclin D1 were significantly different among three groups (P<0.01 or <0.05). The KAI1/CD82 expression in patients with TNM stage III-IV LSCC, poorly differentiated LSCC, clinical stage III-IV LSCC or lymph node metastasis was markedly lower than that in those with TNM stage I-II LSCC, well differentiated LSCC, clinical stage I-II LSCC or no lymph node metastasis (P<0.01 or <0.05). However, there was no marked difference in KAI1/CD82 expression between males and females and among patients in different age groups (P>0.05). In LSCC patients positive for KAI1/CD82 protein expression, the median survival time was 76 months, which was significantly longer than that in LSCC patients negative for KAI1/CD82 protein expression (48 months; X(2)=16.293, P=0.000). The Cyclin D1 expression in patients with TNM stage III-IV LSCC, poorly differentiated LSCC, or clinical stage III-IV LSCC was dramatically higher than that in patients with TNM stage I-II LSCC, well differentiated LSCC, or clinical stage I-II LSCC (P<0.01 or <0.05). However, no marked difference was noted in cyclin D1 expression between males and females, among patients in different age groups and between patients with and without lymph node metastasis (P>0.05). In LSCC patients positive for cyclin D1 protein expression, the median survival time was 40 months, which was markedly shorter than that in LSCC patients negative for cyclin D1 protein expression (X(2)=9.517, P=0.02). In LSCC patients, there was a negative correlation between KAI1/CD82 expression and cyclin D1 expression (X(2)=7.86, P<0.01).
CONCLUSION: KAI1/CD82 affects cell cycle. Both KAI1/CD82 and cyclin D1 are involved in the occurrence and development of LSCC, and may provide clinical information for evaluation of invasiveness, metastasis and prognosis of LSCC. Thus, KAI1/CD82 and cyclin D1 may serve as markers for determination of invasiveness, metastasis and prognosis of LSCC.

Markowska J, Bar J, Mądry R, et al.
The expression of BRCA1, P53, KAI1, and Nm23 in ovaries of BRCA1 mutation carriers after prophylactic adnexectomy.
Arch Gynecol Obstet. 2013; 288(4):839-44 [PubMed] Free Access to Full Article Related Publications
INTRODUCTION: High mortality rate, absence of reliable methods for early diagnosis and poor prognosis of advanced ovarian cancer prompted to investigate the role of prophylactic oophorectomy in BRCA1 mutation carriers as well as evaluate the expression of BRCA1, p53, Nm23, and KAI1 proteins in ovarian tissue from these patients.
MATERIALS AND METHODS: Ovaries from BRCA1 mutation carriers underwent prophylactic adnexectomy and control group of patients were operated from other than cancer reasons. The expression of selected proteins was studied using immunohistochemical staining. The intensity of immunostaining and the number of tumor cells showing the reaction for selected proteins were analyzed.
RESULTS: We have analyzed ovarian tissues from 18 BRCA1 mutation carriers and 11 women included in control group. Positive expression of BRCA1 protein was presented in 83.3 % cases in BRCA1 mutation carriers and in 72.7 % in the control group (p > 0.05). Positive expression of p53 protein was observed, respectively, in 27.8 vs. 36.4 % (p > 0.05), Nm23 protein 77.7 vs. 90.9 % (p > 0.05), and KAI1 in 72.2 vs. 72.7 % (p > 0.05). Mean percent of tumor cells that showed the reaction for selected proteins as well as the intensity of immunostaining for all analyzed proteins seems to be lower in BRCA1 mutation carriers.
CONCLUSIONS: However, any significant differences between study group and control group have not been found; there were similar trends showing reduced expression of studied proteins in BRCA1 mutation carriers.

Risinger JI, Custer M, Feigenbaum L, et al.
Normal viability of Kai1/Cd82 deficient mice.
Mol Carcinog. 2014; 53(8):610-24 [PubMed] Related Publications
The KAI1/CD82 tetraspanin is a widely expressed cell surface molecule thought to organize diverse cellular signaling processes. KAI1/CD82 suppresses metastasis but not tumorigenicity, establishing it as one of a class of metastasis suppressor genes. In order to further assess its functions, we have characterized the phenotypic properties of Kai1/Cd82 deleted mice, including viability, fertility, lymphocyte composition, blood chemistry and tissue histopathology, and of their wild-type and heterozygote littermates. Interestingly, Kai1/Cd82(-/-) showed no obvious genotype associated defects in any of these processes and displayed no genotype associated histopathologic abnormalities after 12 or 18 months of life. Expression profiles of non-immortal, wild-type and Kai1/Cd82(-/-) mouse embryo fibroblast (MEFs) indicated distinct sex-specific and genotype-specific profiles. These data identify 191 and 1,271 differentially expressed transcripts (by twofold at P < 0.01) based on Kai1/CD82 genotype status in female and male MEFs, respectively. Differentially expressed genes in male MEFs were surprisingly enriched for cell division related processes, suggesting that Kai1/Cd82 may functionally affect these processes. This suggests that Kai/Cd82 has an unappreciated role in the early establishment of proliferation and division when challenged with a new environment that might play a role in adaptability to new metastatic sites.

Ji XD, Yan H, Zhao PQ
[Expression changes of tumor metastasis-related genes after overexpression of KAI1 in retinoblastoma Y79 cells].
Zhonghua Yan Ke Za Zhi. 2012; 48(12):1097-101 [PubMed] Related Publications
OBJECTIVE: To investigate the expression changes of tumor metastasis-related genes after overexpression of KAI1 in retinoblastoma Y79 cells.
METHODS: Experimental study. Y79 cells were transfected with a lentivirus vector containing KAI1 and enhanced green fluorescent protein (EGFP) fusion gene, or a control lentivirus vector containing EGFP. Positive transfectants stably expressing high levels of KAI1 were named Y79-KAI1 and control transfectants were named Y79-KAI1/zero. These transfectants were selected by puromycin resistance and analysis with fluorescent microscopy. The expression of KAI1 mRNA and its protein among Y79, Y79-KAI1 and Y79-KAI1/zero were detected by fluorescent quantitative RT-PCR and Western blot. Differential expression of tumor metastasis-related genes in Y79-KAI1 and Y79-KAI1/zero was analyzed with human tumor metastasis PCR array. One-way ANOVA was used to analyze the differences of KAI1 mRNA and protein expression among the three groups.
RESULTS: The stably transfected cell lines of Y79-KAI1 and Y79-KAI1/zero were established. The result of fluorescent quantitative real-time PCR showed that the relative quantification of mRNA level of KAI1 gene in the three kinds of cells above was 183.67 ± 21.20, 1.42 ± 0.55, 1.00 ± 0.00, respectively. And the expression level of KAI1 mRNA in Y79-KAI1 cells was significantly higher than those in Y79-KAI1/zero and Y79 cells (F = 108.74, P = 0.000). The results of Western blot showed that the expression level of the KAI1 protein in Y79-KAI1 cells was significantly higher than those in Y79-KAI1/zero and Y79 cells (F = 34.36, P = 0.001). Immunofluorescent staining showed that Y79 and Y79-KAI1/zero cells had no detectable KAI1 expression, while Y79-KAI1 cells expressed KAI1 in the cytoplasm surrounding the nuclei. Among the 84 tumor metastasis-related genes examined, 7 genes were up-regulated more than 2 folds and 6 genes were down-regulated over 50%.
CONCLUSION: Over-expression of KAI1 may result in differential expression of tumor metastasis-related genes in Y79 cells, which may be related to the inhibitory effect on the tumor metastasis of retinoblastoma.

Guo C, Liu Q, Zhang L, et al.
Double lethal effects of fusion gene of wild-type p53 and JunB on hepatocellular carcinoma cells.
J Huazhong Univ Sci Technolog Med Sci. 2012; 32(5):663-8 [PubMed] Related Publications
This study explored the double lethal effects of pEGFP-C1-wtp53/junB fusion gene on hepatocellular carcinoma (HCC) cells. wtp53/junB fusion gene was constructed and transformed into HepG2 cell line. Expression of KAI1 was detected by quantitative real-time PCR and Western blotting, cells apoptosis rate was detected by flow cytometry, proliferation of cells was detected byMTT chromometry, cell transmigration was detected by using transwell systems. The results showed that after transformation with pEGFP-C1-wtp53/JunB, the expression level of KAI1 protein was up-regulated, being 8.13 times the blank control group in HepG2 cells and significantly higher than 2.87 times which transformed with pEGFP-C1-JunB, 3.11 times which transformed with pEGFP-C1-wtp53 (P<0.001). Apoptosis rate of HepG2 cells transformed with pEGFP-C1-wtp53/JunB was significantly higher than that of other groups (P<0.001), and invasive ability of HepG2 cells transformed with pEGFP-C1-wtp53/JunB was significantly lower than other groups(P<0.001). It was concluded that the fusion gene of wtp53 and JunB could not only inhibit the growth of hepatoma cells and promote tumor cell apoptosis, but also suppress the invasive ability of tumor cells by up-regulating the expression of KAI1.

Saito Y, Kasamatsu A, Yamamoto A, et al.
ALY as a potential contributor to metastasis in human oral squamous cell carcinoma.
J Cancer Res Clin Oncol. 2013; 139(4):585-94 [PubMed] Related Publications
PURPOSE: ALY, an essential mRNA export factor, is dysregulated in a wide variety of human malignancies. However, little is known about the relevance of ALY to oral squamous cell carcinoma (OSCC). The purpose of this study was to investigate ALY expression and its functional mechanisms in OSCCs.
METHODS: ALY mRNA and protein expression in seven OSCC-derived cell lines (Sa3, HO-1-u-1, KON, Ca9-22, HSC-2, HSC-3, and HSC-4) and primary OSCCs were analyzed by quantitative reverse transcriptase-polymerase chain reaction, immunoblotting, and immunohistochemistry. We evaluated cellular invasiveness, migration, and the expression levels of metastasis modulators, ribosomal RNA processing 1 homolog B (RRP1B) and CD82, in ALY knockdown cells.
RESULTS: ALY was frequently up-regulated in OSCC-derived cell lines and primary OSCCs compared with normal counterparts at both the mRNA and protein expression levels. ALY-positive expression was correlated significantly (P < 0.05) with a higher risk of regional lymph node metastasis. Furthermore, ALY knockdown cells caused a significant (P < 0.05) decrease in cellular invasiveness and migration with up-regulation of RRP1B and CD82 compared with the control cells.
CONCLUSION: Our results showed that ALY is linked to regional lymph node metastasis by regulating cellular invasiveness and migration. Therefore, ALY might be a potential biomarker for early detection of lymph node metastasis in OSCCs.

Bonardi F, Fusetti F, Deelen P, et al.
A proteomics and transcriptomics approach to identify leukemic stem cell (LSC) markers.
Mol Cell Proteomics. 2013; 12(3):626-37 [PubMed] Free Access to Full Article Related Publications
Interactions between hematopoietic stem cells and their niche are mediated by proteins within the plasma membrane (PM) and changes in these interactions might alter hematopoietic stem cell fate and ultimately result in acute myeloid leukemia (AML). Here, using nano-LC/MS/MS, we set out to analyze the PM profile of two leukemia patient samples. We identified 867 and 610 unique CD34(+) PM (-associated) proteins in these AML samples respectively, including previously described proteins such as CD47, CD44, CD135, CD96, and ITGA5, but also novel ones like CD82, CD97, CD99, PTH2R, ESAM, MET, and ITGA6. Further validation by flow cytometry and functional studies indicated that long-term self-renewing leukemic stem cells reside within the CD34(+)/ITGA6(+) fraction, at least in a subset of AML cases. Furthermore, we combined proteomics with transcriptomics approaches using a large panel of AML CD34(+) (n = 60) and normal bone marrow CD34(+) (n = 40) samples. Thus, we identified eight subgroups of AML patients based on their specific PM expression profile. GSEA analysis revealed that these eight subgroups are enriched for specific cellular processes.

Shiwu WU, Lan Y, Wenqing S, et al.
Expression and clinical significance of CD82/KAI1 and E-cadherin in non-small cell lung cancer.
Arch Iran Med. 2012; 15(11):707-12 [PubMed] Related Publications
BACKGROUND: This study investigates the expression of CD82/KAI1 and epithelial-cadherin (E-cad) in non-small cell lung cancer (NSCLC).
METHODS: Tissues of resected primary NSCLC and normal lung tissue were investigated. Protein expression was detected with immunohistochemical staining. mRNA expression levels of CD82/KAI1 and E-cad were determined by semiquantitative reverse transcriptase polymerase chain reaction (RT-PCR) after mRNA extraction.
RESULTS: The expression of CD82/KAI1 and E-cad was significantly lower in NSCLC compared to normal lung tissue (P < 0.01). CD82/KAI1 and E-cad mRNA and protein expression were found to be in close relationship with the grade of differentiation, lymph node metastasis and pathologic tumor-node-metastasis (pTNM) stages, and survival in NSCLC (P < 0.01), but no relationship was observed with gender, diameter, type, histological type and age (P > 0.05). Expression of mRNA CD82/KAI1 and E-cad were consistent with their proteins (P < 0.01), and there was a significant relationship between expression of CD82/KAI1 and E-cad. The survival rate of the CD82/KAI1-positive and CD82/KAI1-negative groups was significantly different (P < 0.01). In addition, the survival rate was significantly different between the E-cad-positive and E-cad-negative groups. pTNM stages and positive expression of CD82/KAI1 and E-cad were independent prognostic factors of NSCLC (P < 0.05).
CONCLUSION: Lower expression of CD82/KAI1 and E-cad was found in NSCLC compared to normal lung tissue. Decreased expression of CD82/KAI1 and E-cad was closely related to cellular differentiation, pTNM stages, invasion and metastasis.

Chigita S, Sugiura T, Abe M, et al.
CD82 inhibits canonical Wnt signalling by controlling the cellular distribution of β-catenin in carcinoma cells.
Int J Oncol. 2012; 41(6):2021-8 [PubMed] Free Access to Full Article Related Publications
We have recently unravelled a novel function for CD82 in E-cadherin-mediated cellular adhesion. CD82 inhibits β-catenin tyrosine phosphorylation and stabilizes E-cadherin-β-catenin complexes at the cell membrane. This function inhibits cancer cell dissociation from the primary cancer nest and limits metastasis. In this study, we focused on the effect of CD82 on the Wnt/β-catenin (canonical) pathway, which controls the cellular distribution of β-catenin. CD82 had no effect on the expression of Wnt proteins but led to significant downregulation of Frizzled (Fzd) 2, 3, 5, 7 and 9, suggesting downregulation of the Wnt/β-catenin pathway. CD82 also inhibited phosphorylation of β-catenin at Ser45, Ser33, Ser37 and Thr41 by downregulation of glycogen synthase kinase-3β (GSK-3β) and kinase casein kinase 1α (CK1α). Downregulation of GSK-3β and CK1α also led to accumulation of β-catenin in the cytoplasm or at the cell membrane. CD82 translocated β-catenin to the cell membrane, suggesting that CD82 strengthens the interaction between E-cadherin and β-catenin. We concluded that CD82 attenuates Wnt signalling by controlling β-catenin cellular distribution at multiple levels: i) inhibition of β-catenin nuclear translocation by downregulation of Fzd receptor proteins; ii) accumulation of β-catenin at the cell membrane by downregulation of GSK-3β and CK1α; and iii) stabilization of the E-cadherin-β-catenin complex.

Nishioka C, Ikezoe T, Furihata M, et al.
CD34⁺/CD38⁻ acute myelogenous leukemia cells aberrantly express CD82 which regulates adhesion and survival of leukemia stem cells.
Int J Cancer. 2013; 132(9):2006-19 [PubMed] Related Publications
To identify molecular targets in leukemia stem cells (LSCs), this study compared the protein expression profile of freshly isolated CD34(+) /CD38(-) cells with that of CD34(+) /CD38(+) counterparts from individuals with acute myelogenous leukemia (n = 2, AML) using isobaric tags for relative and absolute quantitation (iTRAQ). A total of 98 proteins were overexpressed, while six proteins were underexpressed in CD34(+) /CD38(-) AML cells compared with their CD34(+) /CD38(+) counterparts. Proteins overexpressed in CD34(+) /CD38(-) AML cells included a number of proteins involved in DNA repair, cell cycle arrest, gland differentiation, antiapoptosis, adhesion, and drug resistance. Aberrant expression of CD82, a family of adhesion molecules, in CD34(+) /CD38(-) AML cells was noted in additional clinical samples (n = 12) by flow cytometry. Importantly, down-regulation of CD82 in CD34(+) /CD38(-) AML cells by a short hairpin RNA (shRNA) inhibited adhesion to fibronectin via up-regulation of matrix metalloproteinases 9 (MMP9) and colony forming ability of these cells as assessed by transwell assay, real-time RT-PCR, and colony forming assay, respectively. Moreover, we found that down-regulation of CD82 in CD34(+) /CD38(-) AML cells by an shRNA significantly impaired engraftment of these cells in severely immunocompromised mice. Taken together, aberrant expression of CD82 might play a role in adhesion of LSCs to bone marrow microenvironment and survival of LSCs. CD82 could be an attractive molecular target to eradicate LSCs.

Pal'tseva EM, Samofalova OIu, Gorbacheva IuV, Tsar'kov PV
[Expression of some biomarkers in primary colon adenocarcinomas and their lymph node metastases].
Arkh Patol. 2012 Jul-Aug; 74(4):12-8 [PubMed] Related Publications
The samples of colon adenocarcinomas (CAC) and their lymph node metastases from 22 patients were studied. The expression of thymidylate synthase (TS), vascular endothelial growth factor (VEGF), epidermal growth factor receptor (EGFR), E-cadherin, beta-catenin, tenascin C (TN), and KAI-1/CD82 in primary CAC and their lymph node metastases was compared using an immunohistochemical method. The expression of TS, VEGF, EGFR, E-cadherin, TNC, and KAI-1 was statistically significant different in primary CAC and involved lymph nodes. Comparison of the expression of the markers in the pairs of primary CAC and metastasis revealed equal values for TNC and EFGR in 45.5 and 41% of cases, respectively; the number of coincidences in the expression of the other markers was insignificant. Determination of the expression of molecular biological markers in primary CAC and their lymph nodes may serve as a predictor of therapy response and have a prognostic value.

Pal'tseva EM, Samofalova OIu, Gorbacheva IuV, Tsar'kov PV
[Molecular markers of colorectal adrenocarcinoma progression].
Arkh Patol. 2012 Mar-Apr; 74(2):14-8 [PubMed] Related Publications
Colorectal adenocarcinoma and its lymph node metastases from 72 patients and 14 control samples were studied. Expression of adhesive molecules - E-cadherin and beta-catenin, antiadhesive molecule - tenascin C and tumor metastasis suppressor KAI-1 (CD82) were studied by immunohistochemistry. The expression of E-cadherin and beta-catenin, tenascin C and KAI-1 was significantly different in adenocarcinoma and control samples. The expression of E-cadherin, tenascin C and KAI-1 was diverse in primary tumor compared to lymph node metastases. The analysis of current data showed the association of E-cadherin expression with stage of disease and depth of invasion, such as the correlation of beta-catenin nuclear expression and tenascin C expression with depth of adenocarcinoma invasion. These data may be a useful indicator of disease progression.

Yoon TM, Kim SA, Lee JK, et al.
Expression of KITENIN and its association with tumor progression in oral squamous cell carcinoma.
Auris Nasus Larynx. 2013; 40(2):222-6 [PubMed] Related Publications
OBJECTIVE: KAI1 COOH-terminal interacting tetraspanin (KITENIN) contributes to tumor invasion and metastasis in various cancers. The aim of this study was to investigate expression of KITENIN in patients with oral cavity squamous cell carcinoma (SCC) and to determine whether KITENIN affects tumor cell behavior in oral cavity SCC cell line.
METHODS: Western blotting and immunohistochemistry was used to assess alteration of KITENIN expression in human oral cavity SCC and normal oral cavity mucosa. To evaluate the impact of KITENIN knockdown, the cell invasion assay and cell migration assay using small-interfering RNA were performed.
RESULTS: KITENIN protein expression was significantly increased in human oral cavity SCC tissues than in normal oral cavity mucosa by Western blotting. KITENIN immunoreactivity was strongly identified in human oral cavity SCC relative to adjacent normal tissue. Knockdown of KITENIN resulted in significantly reduced cell invasion in human oral cavity SCC cells (p=0.001). Cell migration showed a marked decrease in KITENIN knockdown oral cavity SCC cells compared to the negative control oral cavity SCC cells (p=0.01).
CONCLUSION: KITENIN is associated with tumor invasiveness and metastasis in human oral cavity SCC.

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