Fig. 8

Schematic 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 cells