Open Access

ARTICLE

MicroRNA-92a Promotes Cell Proliferation in Cervical Cancer via Inhibiting p21 Expression and Promoting Cell Cycle Progression

by

* Department of Gynecology, Xiamen Maternal and Child Health Care Hospital, Xiamen, Fujian, P.R. China
† Department of Obstetrics and Gynecology VIP, Xiamen Maternal and Child Health Care Hospital, Xiamen, Fujian, P.R. China
‡ Department of Gynecology and Obstetrics, First Affiliated Hospital of Xiamen University, Xiamen, Fujian, P.R. China
1 These authors provided equal contribution to this work.

Oncology Research 2017, 25(1), 137-145. https://doi.org/10.3727/096504016X14732772150262

Abstract

MicroRNA-92a (miR-92a) generally plays a promoting role in human cancers, but the underlying mechanism in cervical cancer remains unclear. Here we studied the expression and clinical significance of miR-92a in cervical cancer, as well as the regulatory mechanism in the proliferation of cervical cancer cells. Our data indicated that miR-92a was significantly upregulated in cervical cancer tissues compared to their matched adjacent nontumor tissues (ANTs), and the increased miR-92a levels were significantly associated with a higher grade, lymph node metastasis, and advanced clinical stage in cervical cancer. In vitro study revealed that inhibition of miR-92a led to a significant reduction in the proliferation of HeLa cells via induction of cell cycle arrest at the G₁ stage. In contrast, overexpression of miR-92a markedly promoted the proliferation of HeLa cells by promoting cell cycle progression. Further investigation revealed that miR-92a has a negative effect on protein levels, but not the mRNA levels, of p21 in HeLa cells, suggesting that p21 is a direct target of miR-92a. Overexpression of p21 eliminated the promoting effects of miR-92a on the proliferation and cell cycle progression of HeLa cells. However, knockdown of p21 reversed the suppressive effects of miR-92a downregulation on HeLa cell proliferation and cell cycle progression. Moreover, p21 was significantly downregulated in cervical cancer tissues compared to ANTs, suggesting that the increased expression of miR-92a may contribute to the decreased expression of p21, which further promotes cervical cancer growth. In conclusion, our study demonstrates that miR-92a promotes the proliferation of cervical cancer cells via inhibiting p21 expression and promoting cell cycle progression, highlighting the clinical significance of miR-92a in cervical cancer.

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