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EZH2 promotes invasion and tumour glycolysis by regulating STAT3 and FoxO1 signalling in human OSCC cells
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EZH2 promotes invasion and tumour glycolysis by regulating STAT3 and FoxO1 signalling in human OSCC cells
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Journal Article
EZH2 promotes invasion and tumour glycolysis by regulating STAT3 and FoxO1 signalling in human OSCC cells
2019
Overview
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.
Publisher
John Wiley & Sons, Inc,John Wiley and Sons Inc
Subject
/ Antigens
/ Carcinoma, Squamous Cell - genetics
/ Carcinoma, Squamous Cell - metabolism
/ Carcinoma, Squamous Cell - pathology
/ Enhancer of Zeste Homolog 2 Protein - metabolism
/ Epithelial-Mesenchymal Transition - genetics
/ epithelial‐mesenchymal transition
/ Female
/ Forkhead Box Protein O1 - metabolism
/ FoxO1
/ Gene Expression Regulation, Neoplastic
/ Humans
/ invasion
/ Male
/ Mouth Neoplasms - metabolism
/ mRNA
/ Oral squamous cell carcinoma
/ Original
/ Proteins
/ STAT3
/ STAT3 Transcription Factor - metabolism
/ Studies
/ Tumors
