Upregulation of Fas in epithelial ovarian cancer reverses the development of resistance to Cisplatin

This study was to investigate the role of Fas in the development of Cisplatin-resistant ovarian cancer. On the cellular level, Fas expression was significantly reduced in Cisplatin resistant A2780 (A2780/CP) cells compared with A2780 cells. Fas silence with siRNA would promote tumor cell lines proli...

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Veröffentlicht in:BMB reports 2015, 48(1), , pp.30-35
Hauptverfasser: Yang, F., Ningxia People's Hospital, Yinchuan, People's Republic of China, Long, W., Ningxia Medical University, Yinchuan, People's Republic of China, Xuechuan, H., Ningxia People's Hospital, Yinchuan, People's Republic of China, Xueqin, L., Ningxia People's Hospital, Yinchuan, People's Republic of China, Hongyun, M., Ningxia People's Hospital, Yinchuan, People's Republic of China, Yonghui, D., Affiliated Hospital of Ningxia Medical University, Yinchuan, People's Republic of China
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Sprache:eng
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Zusammenfassung:This study was to investigate the role of Fas in the development of Cisplatin-resistant ovarian cancer. On the cellular level, Fas expression was significantly reduced in Cisplatin resistant A2780 (A2780/CP) cells compared with A2780 cells. Fas silence with siRNA would promote tumor cell lines proliferation, facilitate tumor cell cycle transition of G1/S, prevent cell apoptosis, and promote cell migration. Expression of drug resistance gene was negatively correlated to Fas. In nude mice metastasis model of human ovarian carcinoma by subcutaneous transplantation, after Ad-Fas injected intratumorly, we found that upregulation of Fas could inhibit transplantation tumor tissue growth and reduce the expression of drug resistance gene. Our results indicated that upregulation of Fas in epithelial ovarian cancer reversed the development of resistance to Cisplatin. In conclusion, our findings suggested that Fas might act as a promising therapeutic target for improvement of the sensibility to Cisplatin in ovarian cancer.
ISSN:1976-6696
1976-670X
DOI:10.5483/BMBRep.2015.48.1.042