MiR-202 inhibits the progression of human cervical cancer through inhibition of cyclin D1.

Yuexiong Yi,Qing Liu,Wei Zhang,Qiongying Lv,Wenfen Zhang,Juan Zhang,Dingjun Zhu,Kejia Wu,Huirong Li

doi:10.18632/oncotarget.12499

Abstract

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.

Highlights

Cervical cancer act as the second most common tumor among women in this world [1, 2]
We found that SiHa, HeLa, and Caski cell lines had significantly lower expression of miR-202 compared with normal HaCaT cells (Figure 1A)
We examined the existence of miR-202-induced cyclin D1 pathway in CC, and elucidate the significance of miR-202induced cyclin D1 pathway

Summary

Introduction

Cervical cancer act as the second most common tumor among women in this world [1, 2]. It is estimated that about five millions of women patients are newly diagnosed and approximately two millions of cases died of cervical cancer every year. Accumulating evidence showed that human papillomavirus (oncogenic types) plays a crucial role in the induction and development of human cervical cancer [3,4,5]. Some patients did not infect human papillomavirus, suggesting that more potential factors promote the malignant progression of cervical cancer [6,7]. Some related studies were conducted, the molecular etiology of cervical cancer is still largely unknown. We will investigate the molecular mechanisms implicated in the development of cervical cancer

Methods

Results

Conclusion