Back to Search Start Over

Tumor suppression and promotion by autophagy.

Authors :
Ávalos Y
Canales J
Bravo-Sagua R
Criollo A
Lavandero S
Quest AF
Source :
BioMed research international [Biomed Res Int] 2014; Vol. 2014, pp. 603980. Date of Electronic Publication: 2014 Sep 18.
Publication Year :
2014

Abstract

Autophagy is a highly regulated catabolic process that involves lysosomal degradation of proteins and organelles, mostly mitochondria, for the maintenance of cellular homeostasis and reduction of metabolic stress. Problems in the execution of this process are linked to different pathological conditions, such as neurodegeneration, aging, and cancer. Many of the proteins that regulate autophagy are either oncogenes or tumor suppressor proteins. Specifically, tumor suppressor genes that negatively regulate mTOR, such as PTEN, AMPK, LKB1, and TSC1/2 stimulate autophagy while, conversely, oncogenes that activate mTOR, such as class I PI3K, Ras, Rheb, and AKT, inhibit autophagy, suggesting that autophagy is a tumor suppressor mechanism. Consistent with this hypothesis, the inhibition of autophagy promotes oxidative stress, genomic instability, and tumorigenesis. Nevertheless, autophagy also functions as a cytoprotective mechanism under stress conditions, including hypoxia and nutrient starvation, that promotes tumor growth and resistance to chemotherapy in established tumors. Here, in this brief review, we will focus the discussion on this ambiguous role of autophagy in the development and progression of cancer.

Details

Language :
English
ISSN :
2314-6141
Volume :
2014
Database :
MEDLINE
Journal :
BioMed research international
Publication Type :
Academic Journal
Accession number :
25328887
Full Text :
https://doi.org/10.1155/2014/603980