Original Research Article | OPEN ACCESS
Overexpression of MicroRNA-9 inhibits proliferation of human breast cancer cells by targeting STAT3
Yan Zhang ,
Guangquan Dai
Department of Breast Surgery, Affiliated Weihai Second Municipal Hospital of Qingdao University, Weihai264200, PR China;
For correspondence:- Yan Zhang
Email: ZielinskiCanel@yahoo.com Tel:+866315271075
Accepted: 22 August 2018
Published: 30 September 2018
Citation:
Zhang Y, Dai G.
Overexpression of MicroRNA-9 inhibits proliferation of human breast cancer cells by targeting STAT3. Trop J Pharm Res 2018; 17(9):1753-1758
doi:
10.4314/tjpr.v17i9.10
© 2018 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..
Abstract
Purpose: To study the role and therapeutic potential of miR-9 in the treatment of breast cancer.
Methods: The expression of miR-9 was evaluated in breast cancer cell lines using quantitative real-time polymerase chain reaction (qRT-PCR). Proliferation was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, while cell migration was assessed by wound healing assay. Transfections were performed with Lipofectamine 2000 reagent. Overexpression of miR-9 was performed by transfecting breast cancer cells with miR-9 mimics, and suppression of STAT3 was done with Si-RNA construct. Target identification was carried out using target scan, while protein expression was determined with immunoblotting.
Results: The results revealed that miR-9 was significantly (p < 0.05) downregulated in the breast cancer cell lines. Overexpression of miR-9 significantly (p < 0.05) inhibited the proliferation of the breast cancer cells by initiation of apoptosis and cell cycle arrest. In addition, MiR-9 overexpression inhibited the migration of the breast cancer cells. TargetScan analysis showed that STAT3 was the potential target of miR-9: it was significantly downregulated in breast cancer cells overexpressing miR-9. Silencing of STAT3 exerted inhibitory effects on the proliferation and migration of breast cancer cells similar to that of miR-9 overexpression.
Conclusion: MiR-9 regulates the proliferation of human breast cancer by targeting STAT3. Hence, miR-9 can be potentially applied as a therapeutic agent for the management of breast cancer.
Keywords: Breast cancer, MicroRNA-9, STAT3, Apoptosis, Bioinformatic analysis