Premium
Retracted: Micro RNA ‐218 increases cellular sensitivity to R apamycin via targeting R ictor in cervical cancer
Author(s) -
Li Jing,
Li Xiaocui,
Wang Jingpu,
Wang Yuan,
Qiu Haifeng
Publication year - 2015
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/apm.12387
Subject(s) - microrna , cancer research , pi3k/akt/mtor pathway , in vivo , apoptosis , cell growth , biology , cervical cancer , cancer , chemistry , gene , genetics
We previously reported that micro RNA ‐218 was frequently lost in cervical cancer and restoration of micro RNA ‐218 increased cellular radio‐sensitivity via inhibiting. Herein, we aim to investigate the effects of micro RNA ‐218 on cellular response to mTOR inhibition. The expression of micro RNA ‐218 and Rictor were measured by Taqman PCR and real time PCR in a panel of 15 cervical cancer tissues. Micro RNA ‐218 was stably overexpressed in four cervical cancer cell lines and a series of in vitro and in vivo experiments were performed to investigate cellular sensitivity to Rapamycin. In primary cultured cervical cancer cells, the expression of micro RNA ‐218 was negatively correlated with the mRNA level of Rictor, which predicted cellular sensitivity to Rapamycin (p = 0.002, R 2 = 0.6810). In vitro , overexpression of micro RNA ‐218 significantly reduced the level of Rictor and enhanced the growth‐inhibition, cell cycle arrest, and apoptosis induced by Rapamycin. In vivo , overexpression of micro RNA ‐218 further enhanced the suppressive effects of Rapamycin on tumor growth. In conclusion, we demonstrated that micro RNA ‐218 could re‐sensitize cervical cancer to Rapamycin through targeting Rictor. Moreover, patients with loss of micro RNA ‐218 presented notable resistance to Rapamycin, indicating that micro RNA ‐218 might be a valid marker for patients‐stratification in future clinical trials.