Research Papers:
STAT3 is required for MiR-17-5p-mediated sensitization to chemotherapy-induced apoptosis in breast cancer cells
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Abstract
Xing-Hua Liao1,*, Yuan Xiang1,*, Cheng-Xi Yu1,*, Jia-Peng Li1, Hui Li1, Qi Nie1,3, Peng Hu1, Jun Zhou1,4, Tong-Cun Zhang1,2
1Institute of Biology and Medicine, Wuhan University of Science and Technology, Hubei, 430081, P.R. China
2Key Laboratory of Industrial Fermentation Microbiology, Ministry of Education and Tianjin, College of Biotechnology, Tianjin University of Science and Technology, Tianjin, 300457, P.R. China
3Wuhan Medical Treatment Center, Hubei, 430023, P.R. China
4School of Medicine, Wuhan University of Science and Technology, Wuhan, 430065, P.R. China
*These authors have contributed equally to this work
Correspondence to:
Tong-Cun Zhang, email: [email protected]
Xing-Hua Liao, email: [email protected]
Keywords: miR-17-5p, STAT3, paclitaxel, apoptosis, breast cancer
Received: July 02, 2016 Accepted: January 05, 2017 Published: February 02, 2017
ABSTRACT
Signal transducer and activator of transcription 3 (STAT3) controls cell survival, growth, migration, and invasion. Here, we observed that STAT3 exerted anti-apoptotic effects in breast cancer cells. On the other hand, miR-17-5p induced apoptosis in breast cancer cells, and overexpression of miR-17-5p sensitized MCF-7 cells to paclitaxel-induced apoptosis via STAT3. Overexpression of STAT3 in MCF-7 cells decreased paclitaxel-induced apoptosis, but STAT3 knockout abolished the miR-17-5p-induced increases in apoptosis. Finally, miR-17-5p promoted apoptosis by increasing p53 expression, which was inhibited by STAT3. These results demonstrate a novel pathway via which miR-17-5p inhibits STAT3 and increases p53 expression to promote apoptosis in breast cancer cells.
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