STAT3 is required for MiR-17-5p-mediated sensitization to chemotherapy-induced apoptosis in breast cancer cells.
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.
Institute of Biology and Medicine, Wuhan University of Science and Technology, Hubei, 430081, P.R. China.
Xing-Hua
XH
Liao
Institute of Biology and Medicine, Wuhan University of Science and Technology, Hubei, 430081, P.R. China.
Yuan
Y
Xiang
Institute of Biology and Medicine, Wuhan University of Science and Technology, Hubei, 430081, P.R. China.
Cheng-Xi
CX
Yu
Institute of Biology and Medicine, Wuhan University of Science and Technology, Hubei, 430081, P.R. China.
Jia-Peng
JP
Li
Institute of Biology and Medicine, Wuhan University of Science and Technology, Hubei, 430081, P.R. China.
Hui
H
Li
Institute of Biology and Medicine, Wuhan University of Science and Technology, Hubei, 430081, P.R. China.|Wuhan Medical Treatment Center, Hubei, 430023, P.R. China.
Qi
Q
Nie
Institute of Biology and Medicine, Wuhan University of Science and Technology, Hubei, 430081, P.R. China.
Peng
P
Hu
Institute of Biology and Medicine, Wuhan University of Science and Technology, Hubei, 430081, P.R. China.|School of Medicine, Wuhan University of Science and Technology, Wuhan, 430065, P.R. China.
Jun
J
Zhou
Institute of Biology and Medicine, Wuhan University of Science and Technology, Hubei, 430081, P.R. China.|Key Laboratory of Industrial Fermentation Microbiology, Ministry of Education and Tianjin, College of Biotechnology, Tianjin University of Science and Technology, Tianjin, 300457, P.R. China.
Tong-Cun
TC
Zhang
D020413:3' Untranslated Regions / Q000235:genetics; D000972:Antineoplastic Agents, Phytogenic / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects* / Q000235:genetics; D015153:Blotting, Western; D001943:Breast Neoplasms / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D045744:Cell Line, Tumor; D002470:Cell Survival / Q000187:drug effects / Q000235:genetics; D004965:Estrogen Antagonists / Q000494:pharmacology; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D061986:MCF-7 Cells; D035683:MicroRNAs / Q000235:genetics*; D017239:Paclitaxel / Q000494:pharmacology*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D050796:STAT3 Transcription Factor / Q000235:genetics* / Q000378:metabolism; D013629:Tamoxifen / Q000494:pharmacology; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism
D020413:3' Untranslated Regions; D000972:Antineoplastic Agents, Phytogenic; D004965:Estrogen Antagonists; C524941:MIRN17 microRNA, human; D035683:MicroRNAs; D050796:STAT3 Transcription Factor; D016159:Tumor Suppressor Protein p53; D013629:Tamoxifen; D017239:Paclitaxel
STAT3; apoptosis; breast cancer; miR-17-5p; paclitaxel