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BioMed Research International
Volume 2015 (2015), Article ID 373574, 9 pages
http://dx.doi.org/10.1155/2015/373574
Research Article

miR-193b Modulates Resistance to Doxorubicin in Human Breast Cancer Cells by Downregulating MCL-1

1Department of Surgery, The Women’s Hospital, School of Medicine, Zhejiang University, Hangzhou 310006, China
2School of Electronics and Information Engineering, Tongji University, Shanghai 201804, China
3Department of Clinical Laboratory, Tongde Hospital of Zhejiang Province, 234 Gucui Road, Hangzhou 310012, China
4Department of Ophthalmology, Xinhua Hospital, School of Medicine, Jiaotong University, Shanghai 200092, China

Received 24 March 2015; Revised 14 May 2015; Accepted 24 May 2015

Academic Editor: Franco M. Buonaguro

Copyright © 2015 Jingpei Long et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

MicroRNAs (miRNAs) family, which is involved in cancer development, proliferation, apoptosis, and drug resistance, is a group of noncoding RNAs that modulate the expression of oncogenes and antioncogenes. Doxorubicin is an active cytotoxic agent for breast cancer treatment, but the acquisition of doxorubicin resistance is a common and critical limitation to cancer therapy. The aim of this study was to investigate whether miR-193b mediated the resistance of breast cancer cells to doxorubicin by targeting myeloid cell leukemia-1 (MCL-1). In this study, we found that miR-193b levels were significantly lower in doxorubicin-resistant MCF-7 (MCF-7/DOXR) cells than in the parental MCF-7 cells. We observed that exogenous miR-193b significantly suppressed the ability of MCF-7/DOXR cells to resist doxorubicin. It demonstrated that miR-193b directly targeted MCL-1 3′-UTR (3′-Untranslated Regions). Further studies indicated that miR-193b sensitized MCF-7/DOXR cells to doxorubicin through a mechanism involving the downregulation of MCL-1. Together, our findings provide evidence that the modulation of miR-193b may represent a novel therapeutic target for the treatment of breast cancer.