1. EZH2-mediated epigenetic suppression of EphB3 inhibits gastric cancer proliferation and metastasis by affecting E-cadherin and vimentin expression.
- Author
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Zhao K, He J, Wang YF, Jin SD, Fan Y, Fang N, Qian J, Xu TP, and Guo RH
- Subjects
- Cadherins genetics, Cell Line, Tumor, Disease-Free Survival, Enhancer of Zeste Homolog 2 Protein genetics, Epithelial-Mesenchymal Transition, Female, Humans, Male, Middle Aged, Neoplasm Invasiveness, Neoplasm Metastasis, Receptor, EphB3 genetics, Stomach Neoplasms genetics, Stomach Neoplasms mortality, Stomach Neoplasms pathology, Survival Rate, Vimentin genetics, Cadherins biosynthesis, Cell Proliferation, Enhancer of Zeste Homolog 2 Protein metabolism, Epigenesis, Genetic, Gene Expression Regulation, Neoplastic, Receptor, EphB3 biosynthesis, Stomach Neoplasms metabolism, Vimentin biosynthesis
- Abstract
EphB3 is a member of the EPH family of receptors and has been found to play a role in the carcinogenesis of some human cancers. However, its expression and clinical significance in gastric cancer (GC) have not been well documented. In the present study, we detected the expression of EphB3 in GC and adjacent noncancerous tissues and explored its relationships with the clinicopathological features and prognosis of GC patients. It was found that EphB3 silenced GC cells epigenetically by direct transcriptional repression of GC cells via polycomb group protein EZH2 mediation. EphB3 was downregulated in GC cells and tissues, and EphB3 depletion promoted GC cell growth and invasion, while ectopic overexpression of EphB3 produced a significant anti-tumor effect. EphB3 was found to be involved in epithelial-mesenchymal transition by regulating E-cadherin and vimentin expression. In addition, patients with reduced EphB3 expression had shorter disease-free survival (DFS), indicating that EphB3 may prove to be a biomarker for prognosis of GC. These results demonstrated that EphB3 functioned as a tumor-suppressor and prognostic biomarker in GC., (Copyright © 2018 Elsevier B.V. All rights reserved.)
- Published
- 2019
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