Startseite MicroRNA-544 down-regulates both Bcl6 and Stat3 to inhibit tumor growth of human triple negative breast cancer
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MicroRNA-544 down-regulates both Bcl6 and Stat3 to inhibit tumor growth of human triple negative breast cancer

  • Zhengzhi Zhu , Shengying Wang , Jinhai Zhu , Qifeng Yang , Huiming Dong EMAIL logo und Jiankang Huang EMAIL logo
Veröffentlicht/Copyright: 16. Mai 2016

Abstract

Triple negative breast cancer lacking estrogen receptor (ER), progesterone receptor and Her2 account for account for the majority of the breast cancer deaths, due to the lack of specific gene targeted therapy. Our current study aimed to investigate the role of miR-544 in triple negative breast cancer. Endogenous levels of miR-544 were significantly lower in breast cancer cell lines than in human breast non-tumorigenic and mammary epithelial cell lines. We found that miR-544 directly targeted the 3′-untranslated region (UTR) on both Bcl6 and Stat3 mRNAs, and overexpression of miR-544 in triple negative breast cancer cells significantly down-regulated expressions of Bcl6 and Stat3, which in turn severely inhibited cancer cell proliferation, migration and invasion in vitro. Employing a mouse xenograft model to examine the in vivo function of miR-544, we found that expression of miR-544 significantly repressed the growth of xenograft tumors. Our current study reported miR-544 as a tumor-suppressor microRNA particularly in triple negative breast cancer. Our data supported the role of miR-544 as a potential biomarker in developing gene targeted therapies in the clinical treatment of triple negative breast cancer.

Acknowledgments

This work was supported by Anhui Provincial Department of Education (KJ2013Z214).

  1. Conflict of interest statement: The authors have declared that no competing interests exist.

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Supplemental Material:

The online version of this article (DOI: 10.1515/hsz-2016-0104) offers supplementary material, available to authorized users.


Received: 2016-1-8
Accepted: 2016-5-9
Published Online: 2016-5-16
Published in Print: 2016-10-1

©2016 Walter de Gruyter GmbH, Berlin/Boston

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