EZH2 promotes invasion and tumour glycolysis by regulating STAT3 and FoxO1 signalling in human OSCC cells.
Min ZhengMing-Xin CaoXiao-Jie LuoLi LiKe WangSha-Sha WangHao-Fan WangYa-Jie TangYa-Ling TangXin-Hua LiangPublished in: Journal of cellular and molecular medicine (2019)
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.
Keyphrases
- induced apoptosis
- transcription factor
- epithelial mesenchymal transition
- signaling pathway
- long non coding rna
- long noncoding rna
- cell proliferation
- cell cycle arrest
- poor prognosis
- pi k akt
- endothelial cells
- binding protein
- endoplasmic reticulum stress
- type diabetes
- ejection fraction
- newly diagnosed
- induced pluripotent stem cells
- prognostic factors
- drug delivery
- skeletal muscle
- young adults
- high fat diet induced