Influence of 17AAG on proliferation and invasion of gastric cancer cell and its mechanism.
- Author:
Yuehong CUI
1
;
Yiyi YU
;
Tianshu LIU
;
Qian XIE
;
Weizhong WU
;
Kangda LIU
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; Benzoquinones; pharmacology; Cell Cycle; Cell Line, Tumor; Cell Proliferation; drug effects; HSP70 Heat-Shock Proteins; HSP90 Heat-Shock Proteins; Humans; Lactams, Macrocyclic; pharmacology; Neoplasm Invasiveness; Stomach Neoplasms; pathology
- From: Chinese Journal of Gastrointestinal Surgery 2014;17(10):1031-1035
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of 17-allylamino-demethoxygeldanamycin (17AAG) on the proliferative and invasive ability of gastric cancer cells and associated mechanism.
METHODSThe proliferative ability was tested by MTT method and the cell cycle was detected by flow cytometry(FCM) when 17AAG was used to treat gastric cancer cell SGC7901. Apoptosis was detected by FCM and PI-Annexin V double staining. The invasive ability was tested by transwell method. Expression of HSP90, HSP70, c-met and AKT was detected by Western blot.
RESULTSThe growth of SGC7901 cells was inhibited after the administration of 17AAG, and the inhibitation was dose- and time-dependent. The cell cycle was blocked at the G0/G1 phase. The apoptotic ratio in 17AAG group was much higher than that in blank group and DMSO group (P<0.01). The cellular invasive ability decreased significantly (P<0.01). The expression of HSP70 was elevated by 17AAG, and the expression of c-met and AKT was down-regulated, but no change of HSP90 was observed.
CONCLUSION17AAG can inhibit the proliferative and invasive ability of SGC7901 cells, and induces apoptosis through down-regulating the expression of HSP90 client proteins instead of the target HSP90 itself.
