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.
Highlights
Signal transducer and activator of transcription 3 (STAT3) is an important transcription factor [1]
These results demonstrate a novel pathway via which miR-17-5p inhibits STAT3 and increases p53 expression to promote apoptosis in breast cancer cells
We investigated the role of miR-17-5p, which may repress the translation of the STAT3 oncogene, in the control of breast cancer cell apoptosis
Summary
Signal transducer and activator of transcription 3 (STAT3) is an important transcription factor [1]. Several studies have demonstrated that miRNAs play important roles in human cancer [6,7,8,9,10], and miR-17-5p is important in breast cancer. The miR-17-5p cluster acts as a tumor suppressor by directly inhibiting the expression of AIB1 and cyclin D1 in human breast cancer [11, 12]. Yu et al demonstrated that the miR17-5p cluster mediates migration and invasion in breast cancer cells by affecting the secretion of a heterotypic signal [13]. We investigated the role of miR-17-5p, which may repress the translation of the STAT3 oncogene, in the control of breast cancer cell apoptosis
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
