期刊
ONCOTARGET
卷 6, 期 5, 页码 3268-3279出版社
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.3065
关键词
Paclitaxel; miR-125b; EMT; invasion; breast cancer
资金
- National Natural Science Foundation of China [81071848, 81172087]
- priority academic program development of Jiangsu higher education institutions
- Anhui Educational Committee [KJ2013A184]
- Natural Science Foundation of Anhui [1508085MH159]
- Program for graduates research of Bengbu Medical College [Byycx1412]
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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