title: Upregulation of Fas in epithelial ovarian cancer reverses the development of resistance to cisplatin.
abstract: 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.
authors.affiliation: Department of Obstetrics and Gynecology, Ningxia People's Hospital, Yinchuan 750002, People's Republic of China.
authors.forename: Fan
authors.initials: F
authors.lastname: Yang
authors.affiliation: Ningxia Medical University, Yinchuan 750004, People's Republic of China.
authors.forename: Wang
authors.initials: W
authors.lastname: Long
authors.affiliation: Department of Obstetrics and Gynecology, Ningxia People's Hospital, Yinchuan 750002, People's Republic of China.
authors.forename: Han
authors.initials: H
authors.lastname: Xuechuan
authors.affiliation: Department of Obstetrics and Gynecology, Ningxia People's Hospital, Yinchuan 750002, People's Republic of China.
authors.forename: Liu
authors.initials: L
authors.lastname: Xueqin
authors.affiliation: Department of Obstetrics and Gynecology, Ningxia People's Hospital, Yinchuan 750002, People's Republic of China.
authors.forename: Ma
authors.initials: M
authors.lastname: Hongyun
authors.affiliation: Affiliated Hospital of Ningxia Medical University, Yinchuan 750004, People's Republic of China.
authors.forename: Ding
authors.initials: D
authors.lastname: Yonghui
mesh_terms: D020168:ATP Binding Cassette Transporter, Subfamily B, Member 1 / Q000378:metabolism; D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D017209:Apoptosis / Q000187:drug effects; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000187:drug effects; D002945:Cisplatin / Q000494:pharmacology* / Q000627:therapeutic use; D019008:Drug Resistance, Neoplasm; D005260:Female; D059585:G1 Phase Cell Cycle Checkpoints / Q000187:drug effects; D006801:Humans; D051379:Mice; D008819:Mice, Nude; D000089762:Multidrug Resistance-Associated Protein 2; D027425:ATP-Binding Cassette, Sub-Family C Proteins / Q000378:metabolism; D010051:Ovarian Neoplasms / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D034622:RNA Interference; D034741:RNA, Small Interfering / Q000378:metabolism; D014183:Transplantation, Heterologous; D015854:Up-Regulation; D020394:Vault Ribonucleoprotein Particles / Q000378:metabolism; D019014:fas Receptor / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D000099187:Major Vault Protein
chemical_list: D020168:ATP Binding Cassette Transporter, Subfamily B, Member 1; D000970:Antineoplastic Agents; D002945:Cisplatin; D000089762:Multidrug Resistance-Associated Protein 2; D027425:ATP-Binding Cassette, Sub-Family C Proteins; D034741:RNA, Small Interfering; D020394:Vault Ribonucleoprotein Particles; D019014:fas Receptor; D000099187:Major Vault Protein; C491901:FAS protein, human
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