Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2530051 | Current Opinion in Pharmacology | 2011 | 7 Pages |
Autophagy is a mechanism for the degradation of cytoplasmic material, damaged organelles and aggregate-prone proteins in lysosomes. Recent evidence indicates that autophagy is a tumor suppressor mechanism, which is connected to its role in the clearance of the scaffold protein p62/SQSTM1 and prevention of oxidative stress and genomic instability. However, since autophagy is a survival mechanism, cancer cells can also exploit it to survive nutrient limitation and hypoxia that often occur in solid tumors. Tumor cells can also upregulate autophagy as a response to cancer treatment, and recent studies show that inhibition of autophagy can enhance the killing of tumor cells after treatment. Interestingly, the FK506-binding protein 51 plays a role in the autophagy-linked radiation resistance of malignant melanoma.
► In autophagy, cells can deliver their own cytoplasm to lysosomes for degradation. ► Autophagy delivers nutrients during stresses such as starvation and hypoxia. ► Autophagy prevents tumorigenesis by degrading the scaffold protein p62/SQSTM1. ► Established tumor cells can activate autophagy to survive stress and cancer treatment. ► FKBP51 is upregulated in melanoma and enhances radiation-induced autophagy.