Open AccessEZH2 promotes invasion and tumour glycolysis by regulating STAT3 and FoxO1 signalling in human OSCC cells
Author(s) -
Zheng Min,
Cao Mingxin,
Luo Xiaojie,
Li Li,
Wang Ke,
Wang Shasha,
Wang Haofan,
Tang Yajie,
Tang Yaling,
Liang Xinhua
Publication year - 2019
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.14579
Subject(s) - ezh2 , gene silencing , cancer research , stat3 , epithelial–mesenchymal transition , ectopic expression , glycolysis , biology , oncogene , small interfering rna , transfection , cell , metastasis , cancer , phosphorylation , cell culture , cell cycle , gene expression , microbiology and biotechnology , metabolism , gene , endocrinology , biochemistry , genetics
The enhancer of zeste homolog 2 (EZH2), known as a member of the polycomb group (PcG) proteins, is an oncogene overexpressed in a variety of human cancers. Here, we found that EZH2 correlated with poor survival of oral squamous cell carcinoma (OSCC) patients using immunohistochemistry staining. EZH2 overexpression led to a significant induction in tumour glycolysis, Epithelial‐mesenchymal transition (EMT), migration and invasion of OSCC cells. Conversely, silencing of EZH2 inhibited tumour glycolysis, EMT, migration and invasion in OSCC cells. Ectopic overexpression of EZH2 increased phosphorylation of STAT3 at pY705 and decreased FoxO1 expression, and FoxO1 expression was enhanced when inhibiting STAT3. In addition, EZH2 overexpression led to a significant decrease in FoxO1 mRNA levels in nude mice xenograft. These results indicated that regulation of EZH2 might have the potential to be targeted for OSCC treatment.