MiR-125b regulates epithelial-mesenchymal transition via targeting Sema4C in paclitaxel-resistant breast cancer cells
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Qingling Yang1,*, Yangyang Wang2,*, Xiaohui Lu2,*, Zunlan Zhao2, Lihua Zhu2, Sulian Chen1, Qiong Wu3, Changjie Chen1 and Zhiwei Wang4
1 Department of Biochemistry and Molecular Biology, Bengbu Medical College, Anhui, China
2 Clinical Testing and Diagnose Experimental Center of Bengbu Medical College, Anhui, China
3 Department of Medical Oncology, First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui, China
4 Cyrus Tang Hematology Center, Jiangsu Institute of Hematology, Collaborative Innovation Center of Hematology, First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China
* These authors contributed equally to this work
Changjie Chen, email:
Zhiwei Wang, email:
Keywords: Paclitaxel, miR-125b, EMT, invasion, breast cancer
Received: November 20, 2014 Accepted: December 14, 2014 Published: December 18, 2014
Emerging evidence has demonstrated that microRNAs (miRNA) play a critical role in chemotherapy-induced epithelial-mesenchymal transition (EMT) in breast cancer. However, the underlying mechanism of chemotherapy-mediated EMT has not been fully understood. To address this concern, we explored the role of miR-125b in regulation of EMT in stable paclitaxel-resistant (PR) breast cancer cells, namely MCF-7 PR and SKBR3 PR, which have displayed mesenchymal features. Our results illustrated that miR-125b was significantly downregulated in PR cells. Moreover, ectopic expression of miR-125b by its mimics reversed the phenotype of EMT in PR cells. Furthermore, we found that miR-125b governed PR-mediate EMT partly due to governing its target Sema4C. More importantly, overexpression of miR-125b or depletion of Sema4C sensitized PR cells to paclitaxel. These findings suggest that up-regulation of miR-125b or targeting Sema4C could serve as novel approaches to reverse chemotherapy resistance in breast cancers.
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