NDLI: Rab25 is responsible for phosphoinositide 3-kinase/AKTmediated cisplatin resistance in human epithelial ovarian cancer cells.

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Rab25 is responsible for phosphoinositide 3-kinase/AKTmediated cisplatin resistance in human epithelial ovarian cancer cells.

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Rab25 is responsible for phosphoinositide 3-kinase/AKTmediated cisplatin resistance in human epithelial ovarian cancer cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Wang, Long Liu, Xueqin Ma, Hongyun Fan, Yang Han, Xuechuan
Description	Author Affiliation: Fan Y ( Department of Obstetrics and Gynecology, Ningxia People's Hospital, Yinchuan, Ningxia 750000, P.R. China.); Wang L ( Department of Stomatology, Ningxia Medical University, Yinchuan, Ningxia 750004, P.R. China.); Han X ( Department of Obstetrics and Gynecology, Ningxia People's Hospital, Yinchuan, Ningxia 750000, P.R. China.); Liu X ( Department of Obstetrics and Gynecology, Ningxia People's Hospital, Yinchuan, Ningxia 750000, P.R. China.); Ma H ( Department of Obstetrics and Gynecology, Ningxia People's Hospital, Yinchuan, Ningxia 750000, P.R. China.)
Abstract	Rab25, a member of the Rab family of small guanosine triphosphatase, was reported to have an essential role in the development of human epithelial ovarian cancer. The present study demonstrated that Rab25 mediated the sensitivity of ovarian cancer to cisplatin, a firstline chemotherapeutic agent for the treatment of ovarian cancer in the clinic. Overexpression of Rab25 and increased phosphoinositide 3kinase (PI3K)/AKT signaling were detected in cisplatinresistant SKOV3 cells compared with those in cisplatinsensitive ES2 cells. The results of the present study indicated that cisplatin resistance was primarily due to reduced G1 cell cycle arrest following cisplatin treatment in SKOV3 cells. By contrast, the corresponding phenomenon was not observed following treatment with a Rab25specific small interfering RNA or treatment with the PI3K/AKT inhibitor LY294002. Of note, inhibition of the PI3K/AKT pathway reduced Rab25 gene expression and sensitized SKOV3 cells to cisplatin. Furthermore, knockdown of Rab25 showed an effect comparable with blocking the PI3K/AKT pathway. In conclusion, the results of the present study demonstrated that PI3K/AKT and Rab25 significantly contributed to cisplatin resistance in human epithelial ovarian cancer; in addition, silencing Rab25 or inhibiting the PI3K/AKT pathway markedly increased the sensitivity of these cells to cisplatin.
ISSN	17912997
e-ISSN	17913004
Journal	Molecular Medicine Reports
Issue Number	3
Volume Number	11
Language	English
Publisher	Spandidos Publications
Publisher Date	2015-03-01
Publisher Place	Greece
Access Restriction	Open
Subject Keyword	Drug Resistance, Neoplasm Genetics Neoplasms, Glandular And Epithelial Metabolism Ovarian Neoplasms Phosphatidylinositol 3-kinases Proto-oncogene Proteins C-akt Rab Gtp-binding Proteins Antineoplastic Agents Pharmacology Apoptosis Drug Effects Cell Line, Tumor Cisplatin G1 Phase Cell Cycle Checkpoints Gene Expression Gene Knockdown Techniques Rna, Small Interfering Signal Transduction Research Support, Non-u.s. Gov't Discipline Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology

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