Dataset Information

Reduced E-cadherin facilitates renal cell carcinoma progression by WNT/?-catenin signaling activation.

ABSTRACT: Reduced expression of E-cadherin was observed in renal cell carcinoma (RCC). However, its potential clinical value and correlation with WNT/?-catenin signaling in RCC progression was still unclear. Immunohistochemical staining was performed in RCC tissue microarray to examine the expression status and prognosis value of E-cadherin and ?-catenin. The potential role of E-cadherin in ?-catenin translocation was analyzed with immunobloting assays. A significant negative correlation was observed between E-cadherin and ?-catenin expression in RCC tissues. E-cadherin inhibits ?-catenin translocation from membrane to cytoplasm in RCC tissues, which was an important step for WNT/?-catenin signaling. Reduced E-cadherin expression was associated with poor prognosis. More importantly, E-cadherin-/?-catenin+ was an independent detrimental factor for survival estimation of RCC patients. Reduced E-cadherin expression in RCC promoted cancer progression via WNT/?-catenin signaling pathway activation. E-cadherin/?-catenin provides a valuable prognosis marker for RCC, which may be an effective target for RCC therapy.

SUBMITTER: Zhang X

PROVIDER: S-EPMC5386706 | biostudies-literature | 2017 Mar

REPOSITORIES: biostudies-literature

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Reduced E-cadherin facilitates renal cell carcinoma progression by WNT/β-catenin signaling activation.

Zhang Xinqi X Yang Mingxi M Shi Hua H Hu Jianxin J Wang Yuanlin Y Sun Zhaolin Z Xu Shuxiong S

Oncotarget 20170301 12

Reduced expression of E-cadherin was observed in renal cell carcinoma (RCC). However, its potential clinical value and correlation with WNT/β-catenin signaling in RCC progression was still unclear. Immunohistochemical staining was performed in RCC tissue microarray to examine the expression status and prognosis value of E-cadherin and β-catenin. The potential role of E-cadherin in β-catenin translocation was analyzed with immunobloting assays. A significant negative correlation was observed betw ...[more]

PMID: 28223537

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Project description:BackgroundHepatocellular carcinoma is a widespread cancer worldwide, ranking as the fifth most frequent cancer and the fourth leading cause of cancer-related deaths. According to comprehensive research, TLK2, a phosphorylated kinase, has been discovered to play a crucial role in promoting tumor development. However, the prognostic significance and influence of TLK2 on hepatocellular carcinoma tumor cells and the immune microenvironment remain unexplored, warranting further investigation. The aim of this study was to investigate the role of TLK2 in promoting the development of hepatocellular carcinoma.MethodsThe present study utilized The Cancer Genome Atlas (TCGA) database and other databases as training sets to examine the expression of TLK2 and its prognostic significance. The findings were subsequently validated through cell proliferation assays and cell colony assays. Gene set enrichment analysis (GSEA) was employed to investigate the tumor-related biological processes associated with TLK2 in hepatocellular carcinoma, while the relationship between TLK2 expression and Wnt/β-catenin signaling pathway was analyzed via TCGA dataset analysis. Western blotting and immunofluorescence assays were used to confirm the experimental results.ResultsTLK2 showed higher expression levels in tumor tissues than in normal tissues. Alpha fetoprotein (AFP), T stage, pathological stage, and histological grade were significantly associated with TLK2 expression. High TLK2 expression correlated with worse overall survival (OS) [hazard ratio (HR) =1.62, 95% confidence interval (CI): 1.14-2.29, P=0.007], progression-free survival (PFS) (HR =1.88, 95% CI: 1.40-2.52, P<0.001) and disease specific survival (DSS) (HR =1.86, 95% CI: 1.18-2.93, P=0.007) in the training and validation sets. Both univariate and multivariate analyses showed that TLK2 was an independent prognostic factor. GSEA showed that TLK2 was significantly enriched in tumor-related biological processes. TLK2 induced the activation of β-catenin signaling, resulting in sustained tumor growth. Methyl thiazolyl tetrazolium (MTT) and colony formation assays demonstrated that TLK2 could promote hepatocellular carcinoma progression. Furthermore, TLK2 showed a significant association with β-catenin in the Wnt pathway.ConclusionsTLK2 represents an independent prognostic factor in hepatocellular carcinoma and can promote cancer progression via the β-catenin signaling pathway.

Dataset Information

Reduced E-cadherin facilitates renal cell carcinoma progression by WNT/?-catenin signaling activation.

Publications

Reduced E-cadherin facilitates renal cell carcinoma progression by WNT/β-catenin signaling activation.

Similar Datasets

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