miR-202 inhibits the progression of human cervical cancer through inhibition of cyclin D1
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Yuexiong Yi1, Huirong Li2, Qiongying Lv1, Kejia Wu1, Wenfen Zhang3, Juan Zhang4, Dingjun Zhu5, Qing Liu3, Wei Zhang1
1Department of Obstetrics and Gynecology, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan 430071, P.R. China
2Department of Gynecology, Shandong Jiaohong Hospital, Jinan, Shandong 250031, P.R. China
3Department of Gynecology, The 5th Hospital of Jinan, Shandong 250031, P.R. China
4The First Department of Gynecology, Renmin Hospital of Wuhan University, Wuhan University, Wuhan 430071, P.R. China
5Department of Gynecology, Shiyan Materal and Children Health Hospital, Shiyan 44200, P.R. China
Wei Zhang, email: firstname.lastname@example.org
Keywords: miR-202, cyclin D1, cervical cancer
Received: June 30, 2016 Accepted: September 28, 2016 Published: October 06, 2016
The human cervical cancer (CC) acts as the most common one of women tumors. However, the pathological changes and molecular alterations of CC are not clear. It has been reported that miR-202 takes part in the development and progression of different tumors. The present study aims to detect the expression of miR-202 in 100 cases of CC tissues and cells, and then we continued to investigate the potential mechanisms of miR-202 in CC cells. In this work, we found that the expression of miR-202 is obviously decreased in both CC cell lines and tissues, and negatively related with the expression of cyclin D1 in SiHa, HeLa and Caski cells. In-vitro assay revealed that the ectopic expression of miR-202 suppressed the proliferation, migration and invasion of SiHa and HeLa cells. Additionally, the over-expression of miR-202 extremely affected the expression of cyclin D1 protein. Notably, the over-expression of cyclin D1 in SiHa and HeLa cells with miR-202 mimics attenuated the inhibitory effects of miR-202 on cell proliferation, migration and invasion. In conclusion, our study identified that miR-202 plays an important role in regulating cell proliferation, migration and invasion of CC by directly targeting cyclin D1, thus miR-202 may represent a potential therapeutic target for patients with cervical cancer.
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