The function of AMPK activation on apoptosis induced by CD437 in cancer cell
10.3760/cma.j.issn.1006-9801.2015.04.001
- VernacularTitle:腺苷酸活化蛋白激酶在维甲酸衍生物CD437介导细胞凋亡中的作用
- Author:
Bin LIANG
;
Xuhong SONG
;
Song YUAN
;
Yanmin LIU
- Publication Type:Journal Article
- Keywords:
Tumor cells;
AMPK;
Apoptosis;
Resistance
- From:
Cancer Research and Clinic
2015;27(4):217-221
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the effects of AMPK activation on cancer cell apoptosis and to investigate the underlying mechanism and its significance to cancer therapy.Methods Human cervical cancer HeLa-S3 cells were divided into six groups:DMSO control,5 μmol/L CD437,CD437+Compound C,CD437+AICAR,Compound C,AICAR.Apoptosis rates in every groups induced by CD437 and other factors were determined by FACS and confirmed with clave Caspase-3 expression by Western blot analysis.Finally,apoptosis rates were detected in HeLa-S3 cells induced by the above factors after wt-LKB1 reintroduction by plasmid transfection.Results FACS results showed that treatment with 5 μmol/L CD437 for 8 hours could induce Hela-S3 cells apoptosis by (87.42±5.95) ％.Co-incubation with 20 μmol/L compound C enhanced apoptotic effect of CD437 by (86.42±5.95) ％,while co-incubation with 2 mmol/L AICAR markedly reduced cell apoptosis induced by CD437 [(51.04±8.26) ％] (P ＜ 0.05).Re-introduction of wt-LKB1 by plasmid transfection attenuated the protective effect of AICAR in CD437 induced apoptosis.Conclusion Endogeneous AMPK activation exerts a protective effect in HeLa-S3 ceils.This effect could be attenuated by re-introduction of wt-LKB1.
