Fig. 5

Employing autophagy against tumors. Basic autophagy recycles dysfunctional or unnecessary proteins and damaged or aged cellular organelles to provide constituent metabolites for cells, and inhibits tumorigenesis. The induction of moderate autophagy by drugs, which possess a higher autophagic flux and triggers drug resistant and even refractory cancer against the induced apoptosis, can be repressed by some chemical inhibitors or therapeutic antibodies (such as RTK inhibitors, AKT inhibitors, proteasome inhibitors, cell cycle inhibitors, miRNA, and EGFR and HER2 therapeutic antibodies). Conversely, other inhibitors (such as mTOR inhibitors, HDAC inhibitors, PARP inhibitors and Bcl-2 inhibitors) and enforced expression of ATG (such as ATG3, ATG4, ATG5, ATG9 and Beclin1) further improve autophagic flux and lead to cell autophagic death due to the excessive autophagy