Fig. 8From: Apatinib triggers autophagic and apoptotic cell death via VEGFR2/STAT3/PD-L1 and ROS/Nrf2/p62 signaling in lung cancerSchematic diagram of how apatinib inhibited NSCLC. Apatinib suppressed cell proliferation, induced cell cycle arrest and apoptosis, and inhibited malignance of NSCLC cells. Mechanistically, apatinib downregulated PD-L1 and c-Myc expression through targeting VEGFR2/STAT3 pathway and induced ROS-triggered autophagy via decreasing Nrf2 and p62 in NSCLC cells. Apatinib further reduced immunosuppressive TME by suppressing PD-L1 expression in tumor-associated macrophages and partially restoring the activation of T cellsBack to article page