Liao Xing-Hua, Xiang Yuan, Yu Cheng-Xi, Li Jia-Peng, Li Hui, Nie Qi, Hu Peng, Zhou Jun, Zhang Tong-Cun
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.
Oncotarget. 2017 Feb 28;8(9):15763-15774. doi: 10.18632/oncotarget.15000.
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.
信号转导及转录激活因子3（STAT3）控制细胞存活、生长、迁移和侵袭。在此，我们观察到STAT3在乳腺癌细胞中发挥抗凋亡作用。另一方面，miR-17-5p诱导乳腺癌细胞凋亡，miR-17-5p的过表达通过STAT3使MCF-7细胞对紫杉醇诱导的凋亡敏感。MCF-7细胞中STAT3的过表达降低了紫杉醇诱导的凋亡，但STAT3基因敲除消除了miR-17-5p诱导的凋亡增加。最后，miR-17-5p通过增加p53表达促进凋亡，而p53表达受到STAT3的抑制。这些结果证明了一条新的途径，通过该途径miR-17-5p抑制STAT3并增加p53表达以促进乳腺癌细胞凋亡。
