Inhibition of Heat Shock Protein Hsp90 Reverses Chemotherapy Resistance of Ovarian Cancer

Aim: To explore the mechanism of Hsp90 in chemotherapy resistance of paclitaxel in ovarian cancer. Methods: MTT were used to detect the effect of BIIB021 on ovarian cancer resistant cells (A2780/Taxol) to paclitaxel, half inhibitory concentration and flow cytometry were used to detect apoptosis. Western blotting was performed to detect MRP1, MDR1, Bcl2 and Survivin protein expression in A2780 and A2780/Taxol treated with Hsp90 inhibitor BIIB021 or transfected pcDNA3.1-Hsp90 and siHsp90. Results: Inhibition of Hsp90 enhanced the inhibitive rates of paclitaxel to A2780/taxol, reduced the IC50, and the expression of MRP1, MDR1, Bcl-2 and Survivin. Apoptosis was significantly increased in A2780/taxol cells treated with BIIB021 and paclitaxel. Furthermore, overexpression of Hsp90 increased MRP1, MDR1, Bcl-2 and Survivin expression while interference of Hsp90 reduced the expression of above. Conclusions: Hsp90 could enhance the chemotherapy sensitivity to paclitaxel in ovarian cancer by inhibiting the expression of Bcl2, MDR1, survivin and MRP1. *Corresponding authors: Kun Zhang, School of Biomedical Sciences, Chengdu Medical College, Chengdu, China, Tel: +86 028 62739585, Fax: +86 028 62739585; E-mail: [email protected] & Minhui Li, School of Basic Medical Sciences, Chengdu Medical College, Chengdu, China, E-mail: [email protected] & He Wei, School of Biomedical Sciences, Chengdu Medical College, Chengdu, China, E-mail: [email protected] Received Date: April 18, 2017 Accepted Date: May 16, 2017 Published Date: May 20, 2017