Journal
ONCOGENE
Volume 35, Issue 3, Pages 323-332Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/onc.2015.84
Keywords
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Funding
- Natural Science Foundation of China [81402165/81301194]
- Natural Science Foundation of Jiangsu Province [BK20131241]
- Clinical Special Projects of Science and Technology Department of Jiangsu Province [BL2012059]
- Research Projects of Jiangsu Provincial Health Department [H201451]
- Maternal and Child Health Research Projects of Jiangsu Province [F201437/F201350/F201215]
- Social Development of Zhenjiang [SH2012057/SH2013025]
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Epithelial-mesenchymal transition (EMT) has an established role in promoting tumor progression and the acquisition of therapeutic resistance. Here, the EMT phenotype was detected in cisplatin-resistant ovarian cancer tissues and cell lines, and correlated with decreased miR-186 expression, increased Twist1 expression, chemoresistance and poor prognosis in epithelial ovarian cancer (EOC) patients. Introducing miR-186 into EOC cells led to a reduction in twist family bHLH transcription factor 1 (Twist1) expression along with morphological, functional and molecular changes consistent with mesenchymal-to-epithelial transition, G1 cell-cycle arrest and enhanced cell apoptosis, which consequently rendered the cells more sensitive to cisplatin in vitro and in vivo. Furthermore, luciferase reporter and rescue assay results showed that the EMT and drug resistance reversal in response to miR-186 was mediated by Twist1. Collectively, these findings implicate miR-186 as an attractive candidate for overcoming chemoresistance in ovarian cancer therapy.
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