作者: Li‐Ping Zeng , Zheng‐Mao Hu , Kai Li , Kun Xia
DOI: 10.1111/JCMM.12760
关键词: Cancer research 、 Programmed cell death 、 PI3K/AKT/mTOR pathway 、 Bladder cancer 、 Medicine 、 Cell growth 、 Protein kinase B 、 RPTOR 、 Cisplatin 、 Protein phosphatase 2
摘要: Increased miR-222 levels are associated with a poor prognosis in patients bladder cancer. However, the role of remains unclear. In present study, we found that enhanced proliferation both T24 and 5637 cancer cell lines. Overexpression attenuated cisplatin-induced death cells. activated Akt/mTOR pathway inhibited autophagy cells by directly targeting protein phosphatase 2A subunit B (PPP2R2A). Blocking activation Akt LY294002 or mTOR rapamycin significantly prevented miR-222-induced restored sensitivity to cisplatin. These findings demonstrate modulates PPP2R2A/Akt/mTOR axis thus plays critical regulating chemotherapeutic drug resistance. Therefore, may be novel therapeutic target for