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Oncotarget. 2017 Feb 28;8(9):15763-15774. doi: 10.18632/oncotarget.15000.

STAT3 is required for MiR-17-5p-mediated sensitization to chemotherapy-induced apoptosis in breast cancer cells.

Author information

1
Institute of Biology and Medicine, Wuhan University of Science and Technology, Hubei, 430081, P.R. China.
2
Wuhan Medical Treatment Center, Hubei, 430023, P.R. China.
3
School of Medicine, Wuhan University of Science and Technology, Wuhan, 430065, P.R. China.
4
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.

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.

KEYWORDS:

STAT3; apoptosis; breast cancer; miR-17-5p; paclitaxel

PMID:
28178652
PMCID:
PMC5362521
DOI:
10.18632/oncotarget.15000
[Indexed for MEDLINE]
Free PMC Article

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