Article
Disruption of the EGFR-SQSTM1 interaction by a stapled peptide suppresses lung cancer via activating autophagy and inhibiting EGFR signaling.
Cancer letters - 1 Apr 2020
Yu Jiao-Jiao, Zhou Dan-Dan, Cui Bing, Zhang Cheng, Tan Feng-Wei, Chang Shan, Li Ke, Lv Xiao-Xi, Zhang Xiao-Wei, Shang Shuang, Xiang Yu-Jin, Chen Fei, Yu Jin-Mei, Liu Shan-Shan, Wang Feng, Hu Zhuo-Wei, Hua Fang
Abstract excerpt
Despite the success of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) in the treatment of non-small cell lung cancer (NSCLC) harboring EGFR-activating mutations, intrinsic or acquired resistance remains the major obstacle to long-term disease remission. Defective autophagy has been reported as an EGFR-TKI resistance mechanism. However, how EGFR regulate autophagic flux are still not...
Read the complete abstract on PubMedTopics
Share this publication in a Topic to start or enrich a Post.
