作者: Tianshu Guo , Ling Xu , Xiaofang Che , Simeng Zhang , Ce Li
DOI: 10.1002/CBIN.10775
关键词:
摘要: Lipid rafts provide a biological platform for apoptosis induced by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). We previously reported that insulin-like growth factor 1 receptor (IGF1R) translocation into lipid helped to explain TRAIL resistance. However, it was not clear whether resistance caused the interaction of IGF1R with caveolin-1 (CAV1) and non-receptor tyrosine kinase SRC in gastric cancer cells. Here, we observed high expression TRAIL-resistant cells, showed combined both CAV1 native complex. shown promote formation IGF1R/CAV1/SRC tri-complex activation these three molecules. Knockdown or inhibition activity reduced this enhanced TRAIL-induced apoptosis. Furthermore, overexpression microRNA-194 reversed reducing expression. In summary, increased downstream survival pathways, leading