Overexpression of STOML-2 inhibits apoptosis of human cervical squamous carcinoma Siha cells in vitro.
- Author:
Guolin HU
1
;
Guangyu YAO
;
Huan DENG
;
Kelei ZHAO
;
Feifei XU
;
Weijiang LIANG
;
Guobing LIU
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; Apoptosis Regulatory Proteins; Blood Proteins; genetics; Carcinoma, Squamous Cell; metabolism; Caspase 3; metabolism; Cell Line, Tumor; Cisplatin; pharmacology; Cytochromes c; metabolism; Female; Flow Cytometry; Humans; Membrane Proteins; genetics; Mitochondria; metabolism; Uterine Cervical Neoplasms; metabolism; bcl-2-Associated X Protein; metabolism
- From: Journal of Southern Medical University 2015;35(9):1293-1296
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the mechanism underlying the inhibitory effect of STOML-2 overexpression on apoptosis of human cervical squamous carcinoma Siha cells.
METHODSSiha cells were transfected with an adenoviral vector carrying STOML-2, and 72 h later STOML-2 expression and the proliferation of the cells were detected by Western blotting and MTT assay. The transfected cells were treated with IC50 Cisplatin for 24 h, and the morphological changes of cells were observed using fluorescence, and the cell apoptosis was analyzed using flow cytomerty; the expression levels of proteins related with mitochondrial apoptosis pathway, including caspase-3, cleaved caspase-3, Bcl-2, Bax and cytochrome C (Cyt C), were detected by Western blotting.
RESULTSWestern blotting showed a significantly increased STOML-2 expression in the transfected cells. Overexpression of STOML-2 obviously promoted the proliferation of Siha cells. The STOML-2-overexpressing cells exhibited an obvious resistance to IC50 Cisplatin-induced apoptosis as shown by both fluorescence microscopy and flow cytometry and presented with decreased expressions of cleaved caspase-3, Bax, and cytosol Cyt C and increased expressions of caspase-3, Bcl-2, and mitochondrial Cyt C.
CONCLUSIONSOverexpression of STOML-2 can enhance the proliferation of Siha cells by inhibiting cell apoptosis possibly through the mitochondrial apoptosis pathway.