Journal
ONCOTARGET
Volume 8, Issue 9, Pages 15763-15774Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.15000
Keywords
miR-17-5p; STAT3; paclitaxel; apoptosis; breast cancer
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Funding
- National Natural Science Foundation of China [31501149, 31570764, 31401117, 31471282, 31440038, 31270837]
- Hubei Province health and family planning scientific research project [WJ2017M173]
- Science and Technology Young Training Program of the Wuhan University of Science and Technology [2016xz035]
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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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