EZH2 plays a role in HSC-T6 cell proliferation and activation affecting MAPK/ERK and PI3 K/AKT pathway
10.3969/j.issn.1001-1978.2015.08.007
- VernacularTitle:EZH2对HSC-T6细胞增殖活化的影响及其部分机制研究
- Author:
Xiaoxia CHEN
;
Juan XIE
;
Cheng HUNANG
;
Xiaoming MENG
;
Jun LI
- Publication Type:Journal Article
- Keywords:
histone methylation;
hepatic stellate cells;
enhancer of zeste homolog 2;
3-deazaneplanocin A;
hepatic fibrosis;
p-ERK;
p-AKT;
alpha-smooth muscle actin
- From:
Chinese Pharmacological Bulletin
2015;(8):1061-1065
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the effects of cell pro-liferation and activation in HSC-T6 cells by inhibiting the expression of EZH2 , and its partial relevant mech-anism. Methods By introducing the inhibitor DZNep in activated HSC-T6 cells stimulated by TGF-β1 , the protein expression levels of EZH2, p-ERK, p-AKT andα-SMA were detected by Western blot. The siRNA targeting EZH2 was designed and synthesized according to its nucleotide sequence, and their corresponding ex-pression vectors were constructed and transfected into HSC-T6 cells with LipofectamineTM 2000. The prolifer-ation of HSC-T6 cells was determined by MTT. And the protein expression levels of EZH2, p-ERK, p-AKT and α-SMA were measured by Western blot. Results By introducing the inhibitor DZNep in activated HSC-T6 cells stimulated by TGF-β1 , it effectively de-creased the protein levels of EZH2 and also the protein levels of p-ERK, p-AKT and α-SMA. By introducing EZH2-siRNA in activated HSC-T6 cells, it effectively inhibited the cell proliferation, and also the protein levels of EZH2, p-ERK, p-AKT andα-SMA. Conclu-sion Silencing EZH2 expression inhibits HSC-T6 cell proliferation and activation, and EZH2 may be a poten-tial therapeutic target gene for hepatic fibrosis.
