A1 Refereed original research article in a scientific journal
The dual role of autophagy in cancer
Authors: Eskelinen EL
Publisher: ELSEVIER SCI LTD
Publication year: 2011
Journal:: Current Opinion in Pharmacology
Journal name in source: CURRENT OPINION IN PHARMACOLOGY
Journal acronym: CURR OPIN PHARMACOL
Volume: 11
Issue: 4
First page : 294
Last page: 300
Number of pages: 7
ISSN: 1471-4892
DOI: https://doi.org/10.1016/j.coph.2011.03.009
Abstract
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.
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.
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