Overexpression of microRNA-132 enhances the radiosensitivity of cervical cancer cells by down-regulating Bmi-1
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Gui-Feng Liu1, Shu-Hua Zhang2, Xue-Feng Li3, Li-Yan Cao1, Zhan-Zhao Fu2 and Shao-Nan Yu1
1Department of Radiology, China-Japan Union Hospital of Jilin University, Changchun 130033, P.R. China
2Operating Room, China-Japan Union Hospital of Jilin University, Changchun 130033, P.R. China
3Department of Anesthesiology, China-Japan Union Hospital of Jilin University, Changchun 130033, P.R. China
Shao-Nan Yu, email: email@example.com
Keywords: microRNA-132, Bmi-1, cervical cancer, HeLa cell, radiosensitivity
Received: December 14, 2016 Accepted: May 21, 2017 Published: August 18, 2017
We examined the effects of microRNA-132 (miR-132) on Bmi-1 expression and radiosensitivity in HeLa, SiHa, and C33A cervical cancer (CC) cells and 104 CC patients. MiR-132 expression was decreased and Bmi-1 expression was increased in tumor tissues compared to adjacent normal tissues and in radiotherapy-resistant patients compared to radiotherapy-sensitive patients. MiR-132 expression and Bmi-1 mRNA expression were also negatively correlated in tumor tissues. HeLa, SiHa, and C33A cells were divided into blank, miR-132 negative control (NC), miR-132 inhibitor, miR-132 mimics, siBmi-1, and miR-132 inhibitor + siBmi-1 groups, after which expression of miR-132 and Bmi-1, and the interaction between them and cell survival, proliferation, and apoptosis were examined. Bmi-1 was confirmed as a target of miRNA-132. Survival was higher and apoptosis lower in the miR-132 inhibitor group than the blank group after various doses of radiation. By contrast, survival was lower and apoptosis higher in the miRNA-132 mimics and siBmi-1 groups than in the blank group. Moreover, miR-132 expression increased and Bmi-1 mRNA expression decreased in each group at radiation doses of 6 and 8 Gy. Finally, co-administration of radiotherapy and exogenous miR-132 inhibited the growth of HeLa cell transplant-induced tumors in nude mice more effectively than radiotherapy alone. These results suggest overexpression of miR-132 enhances the radiosensitivity of CC cells by down-regulating Bmi-1 and that miR-132 may be a useful new target for the treatment of CC.
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