Role of Smac in cisplatin-induced apoptosis of non-small cell lung cancer cells.
- Author:
Xian-dong CHENG
1
;
Shao-xi CAI
;
Hai-jin ZHAO
;
Wen-jun LI
;
Wan-cheng TONG
Author Information
- Publication Type:Journal Article
- MeSH: Antineoplastic Agents; pharmacology; Apoptosis; drug effects; Blotting, Western; Carcinoma, Non-Small-Cell Lung; genetics; metabolism; pathology; Cell Line, Tumor; Cisplatin; pharmacology; Dose-Response Relationship, Drug; Humans; Inhibitor of Apoptosis Proteins; biosynthesis; genetics; Intracellular Signaling Peptides and Proteins; genetics; Lung Neoplasms; genetics; metabolism; pathology; Mitochondrial Proteins; biosynthesis; genetics; RNA, Messenger; biosynthesis; genetics; Reverse Transcriptase Polymerase Chain Reaction
- From: Journal of Southern Medical University 2008;28(3):389-391
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the role of Smac in cisplatin-induced apoptosis of non-small lung cancer cells in vitro.
METHODSNon-small cell lung cancer A549 cells were incubated in the presence of cisplatin at different concentrations, and the cell proliferation status was observed using MTT assay. Flow cytometry was used for evaluation of the apoptosis of the incubated cells, and the expressions of Smac mRNA and protein were detected by RT-PCR and Western blotting, respectively.
RESULTSCisplatin inhibited the proliferation and induced apoptosis of A549 cells both in a concentration-dependent manner. Cisplatin also increased the expression of Smac at both the mRNA and protein levels, which was also concentration-dependent.
CONCLUSIONIncreased Smac expression may play a critical role in cisplatin-induced apoptosis of the non-small cell lung cancer cells in vitro.
