OBJECTIVE: Therapeutic resistance has been a great obstacle for successful treatment of breast cancer. Our study aimed to explore the role of microRNA-760 (miR-760) in chemoresistant breast cancer cells. MATERIALS AND METHODS: Real-time PCR was performed to measure the mRNA expression of miR-760 and Nanog. Western blot was used to determine the protein expression of Nanog and mesenchymal and epithelial markers. Cell viability was measured by the CCK-8 assay. RESULTS: Our results showed that the expression of miR-760 was significantly reduced the doxorubicin (DOX)-resistant MCF-7/DOX cells and chemoresistant breast cancer tissues. Moreover, up-regulation of miR-760 sensitized breast cancer cells to the anti-cancer agents. The MCF-7/DOX cells exhibited increased expression of Snail, a mesenchymal marker, and decreased levels of E-Cadherin, an epithelial marker. In addition, overexpression of miR-760 suppressed the expression of Nanog, a transcriptional factor involved in chemoresistance, and resulted in the reversal of EMT in breast cancer cells. CONCLUSIONS: Our study demonstrated that miR-760 modulated chemoresistance through the epithelial-mesenchymal transition in breast cancer cells, providing a potential therapeutic target for treatment of drug-resistant breast cancer.
OBJECTIVE: Therapeutic resistance has been a great obstacle for successful treatment of breast cancer. Our study aimed to explore the role of microRNA-760 (miR-760) in chemoresistant breast cancer cells. MATERIALS AND METHODS: Real-time PCR was performed to measure the mRNA expression of miR-760 and Nanog. Western blot was used to determine the protein expression of Nanog and mesenchymal and epithelial markers. Cell viability was measured by the CCK-8 assay. RESULTS: Our results showed that the expression of miR-760 was significantly reduced the doxorubicin (DOX)-resistant MCF-7/DOX cells and chemoresistant breast cancer tissues. Moreover, up-regulation of miR-760 sensitized breast cancer cells to the anti-cancer agents. The MCF-7/DOX cells exhibited increased expression of Snail, a mesenchymal marker, and decreased levels of E-Cadherin, an epithelial marker. In addition, overexpression of miR-760 suppressed the expression of Nanog, a transcriptional factor involved in chemoresistance, and resulted in the reversal of EMT in breast cancer cells. CONCLUSIONS: Our study demonstrated that miR-760 modulated chemoresistance through the epithelial-mesenchymal transition in breast cancer cells, providing a potential therapeutic target for treatment of drug-resistant breast cancer.