miR-506: a regulator of chemo-sensitivity through suppression of the RAD51-homologous recombination axis.
10.1186/s40880-015-0049-z
- Author:
Guoyan LIU
1
;
Fengxia XUE
2
;
Wei ZHANG
3
Author Information
1. Department of Gynecology and Obstetrics, Tianjin Medical University General Hospital, Tianjin, 300052, P.R. China. liuguoyan211@126.com.
2. Department of Gynecology and Obstetrics, Tianjin Medical University General Hospital, Tianjin, 300052, P.R. China. fengxiaxue1962@163.com.
3. Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA. wzhang@mdanderson.org.
- Publication Type:Journal Article
- MeSH:
Animals;
Antineoplastic Agents;
Cell Line, Tumor;
Cisplatin;
Disease-Free Survival;
Drug Resistance, Neoplasm;
Drug Therapy, Combination;
Female;
Homologous Recombination;
Humans;
Mice;
MicroRNAs;
Ovarian Neoplasms;
Piperazines;
Prognosis;
Rad51 Recombinase
- From:Chinese Journal of Cancer
2015;34(11):485-487
- CountryChina
- Language:English
-
Abstract:
Ovarian carcinoma is the most lethal gynecologic malignancy. Resistance to platinum is considered the major problem affecting prognosis. Our recent study established that microRNA-506 (miR-506) expression was closely associated with progression-free survival and overall survival in two independent patient cohorts totaling 598 epithelial ovarian cancer cases. Further functional study demonstrated that miR-506 could augment the response to cisplatin and olaparib through targeting RAD51 and suppressing homologous recombination in a panel of ovarian cancer cell lines. Systemic delivery of miR-506 in an orthotopic ovarian cancer mouse model significantly augmented the cisplatin response, thus recapitulating the clinical observation. Therefore, miR-506 plays a functionally important role in homologous recombination and has important therapeutic value for sensitizing cancer cells to chemotherapy, especially in chemo-resistant patients with attenuated expression of miR-506.
