
Simultaneous inhibition of PI3Kα and CDK4/6 synergistically suppresses KRAS-mutated non-small cell lung cancer
Author(s) -
Yuxiang Wang,
Xian Li,
Xueling Li,
Yi Chen,
Chunhao Yang,
Cun Tan,
Bobo Wang,
Yiming Sun,
Xi Zhang,
Yijun Gao,
Jian Ding,
Linghua Meng
Publication year - 2019
Publication title -
cancer biology and medicine
Language(s) - English
Resource type - Journals
ISSN - 2095-3941
DOI - 10.20892/j.issn.2095-3941.2018.0361
Subject(s) - kras , cancer research , pi3k/akt/mtor pathway , cell cycle , cyclin d1 , protein kinase b , cell growth , chemistry , carcinogenesis , cell cycle checkpoint , phosphorylation , cell , signal transduction , cancer , biology , biochemistry , colorectal cancer , genetics
Activating KRAS mutations are the most common drivers in the development of non-small cell lung cancer (NSCLC). However, unsuccess of treatment by direct inhibition of KRAS has been proven. Deregulation of PI3K signaling plays an important role in tumorigenesis and drug resistance in NSCLC. The activity of PI3Kα-selective inhibition against KRAS-mutated NSCLC remains largely unknown.