MicroRNA-183 functions as the tumor suppressor via inhibiting cellular invasion and metastasis by targeting MMP-9 in cervical cancer.
By: Dongmei Fan, Ying Wang, Pengwei Qi, Yawei Chen, Po Xu, Xianan Yang, Ximeng Jin, Xiaoyu Tian

Gynaecology and Obstetrics Department of the First Affiliated Hospital of Henan University of Science and Technology, No. 24 Jinghua Road, Luoyang, Henan 471003, China.
2015-11-21; doi: 10.1016/j.ygyno.2016.02.006
Abstract

Objective

MicroRNAs have been reported to play an important role in the invasion and metastasis of cervical cancer. miR-183 was found to inhibit or promote the invasion and metastasis of multiple solid tumors. However, the roles of miR-183 in cervical cancer are unclear.

Methods

In this study, miR-183 expression levels were measured in 53 cervical cancer and 13 normal cervical tissues by qRT-PCR. The effects of forced expression of miR-183 on cervical cancer cells invasion and metastasis were investigated using Transwell uncoated or coated with growth factor-reduced Matrigel for migration or invasion assays, respectively.

Results

We found that miR-183 expression levels were significantly down-regulated in cervical cancer tissues compared with normal tissues (0.15±0.011 to 0.86±0.049). Ectopic expression of miR-183 resulted in the suppression of invasion and migration of cervical cancer cell lines, siha and Hela cells (p<0.0001). Bioinformatics analysis revealed that MMP-9 was the potential target of miR-183 and it was found that MMP-9 was remarkably up-regulated in cervical cancer. Furthermore, a dual-luciferase reporter assay showed that MMP-9 as a target of miR-183 (p<0.0001). The invasion and metastasis ability of siha and Hela was suppressed when MMP-9 was down-regulated in vitro (p<0.0001).

Conclusions

In conclusion, our study revealed that miR-183 might be a tumor suppressor via inhibiting the invasion and metastasis of cervical cancer cells through targeting MMP-9, indicating that miR-183 may be a novel potential therapeutic target for cervical cancer.



Copyright © 2015. Published by Elsevier Inc.

PMID:26873866






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