RhoE enhances multidrug resistance of gastric cancer cells by suppressing Bax.
We have previously reported that RhoE is overexpressed in the SGC7901/VCR cell line. However, the potential role of RhoE in the development of multidrug resistance of gastric cancer is unknown. In the present study, RhoE enhanced the resistance of SGC7901 cells to several kinds of antitumor drugs. RhoE overexpression did not alter the intracellular adriamycin accumulation of SGC7901 cells nor the expression of P-gp and MRP-1, but protected SGC7901 cells from vincristine-induced apoptosis. RhoE was found to downregulate the expression of Bax at a posttranscriptional level. Western blot revealed no effects of RhoE on the activities of the Caspase family of proteins. In brief, our study demonstrated that RhoE may promote the multidrug resistance phenotype of gastric cancer cells by decreasing the expression of Bax at posttranscriptional level, thus inhibiting vincristine-induced apoptosis.
Li
Kai
K
State Key Laboratory of Cancer Biology and Xijing Hospital of Digestive Diseases, The Fourth Military Medical University, Number 15 Changle Western Road, Xi'an, Shaanxi Province 710032, China.
Lu
Yuanyuan
Y
Liang
Jie
J
Luo
Guanhong
G
Ren
Gui
G
Wang
Xin
X
Fan
Daiming
D
D000970:Antineoplastic Agents / Q000494:pharmacology; D017209:Apoptosis; D045744:Cell Line, Tumor; D018432:Drug Resistance, Multiple; D019008:Drug Resistance, Neoplasm; D006801:Humans; D013274:Stomach Neoplasms / Q000201:enzymology*; D014750:Vincristine / Q000494:pharmacology; D051028:bcl-2-Associated X Protein / Q000037:antagonists & inhibitors*; D020741:rho GTP-Binding Proteins / Q000378:metabolism*
D000970:Antineoplastic Agents; D051028:bcl-2-Associated X Protein; D014750:Vincristine; C508705:RND3 protein, human; D020741:rho GTP-Binding Proteins