title: Tumor suppression and promotion by autophagy.
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.
authors.affiliation: Laboratory of Cellular Communication, Advanced Center for Chronic Diseases (ACCDiS) and Center for Molecular Studies of the Cell, Program in Cell and Molecular Biology, Biomedical Sciences Institute (ICBM), Faculty of Medicine, University of Chile, 8380492 Santiago, Chile ; Laboratory of Molecular Signal Transduction, Advanced Center for Chronic Diseases (ACCDiS) and Center for Molecular Studies of the Cell, Faculty of Chemical and Pharmaceutical Sciences & Faculty of Medicine, University of Chile, 8380492 Santiago, Chile.
authors.forename: Yenniffer
authors.initials: Y
authors.lastname: Ávalos
authors.affiliation: Laboratory of Cellular Communication, Advanced Center for Chronic Diseases (ACCDiS) and Center for Molecular Studies of the Cell, Program in Cell and Molecular Biology, Biomedical Sciences Institute (ICBM), Faculty of Medicine, University of Chile, 8380492 Santiago, Chile.
authors.forename: Jimena
authors.initials: J
authors.lastname: Canales
authors.affiliation: Laboratory of Cellular Communication, Advanced Center for Chronic Diseases (ACCDiS) and Center for Molecular Studies of the Cell, Program in Cell and Molecular Biology, Biomedical Sciences Institute (ICBM), Faculty of Medicine, University of Chile, 8380492 Santiago, Chile ; Laboratory of Molecular Signal Transduction, Advanced Center for Chronic Diseases (ACCDiS) and Center for Molecular Studies of the Cell, Faculty of Chemical and Pharmaceutical Sciences & Faculty of Medicine, University of Chile, 8380492 Santiago, Chile.
authors.forename: Roberto
authors.identifier: 0000-0001-8873-8699
authors.initials: R
authors.lastname: Bravo-Sagua
authors.affiliation: Research Institute of Dental Science, Faculty of Dentistry, University of Chile, 8380492 Santiago, Chile.
authors.forename: Alfredo
authors.initials: A
authors.lastname: Criollo
authors.affiliation: Laboratory of Molecular Signal Transduction, Advanced Center for Chronic Diseases (ACCDiS) and Center for Molecular Studies of the Cell, Faculty of Chemical and Pharmaceutical Sciences & Faculty of Medicine, University of Chile, 8380492 Santiago, Chile ; Department of Internal Medicine, Cardiology Division, University of Texas Southwestern Medical Center, Dallas, TX 75235, USA.
authors.forename: Sergio
authors.identifier: 0000-0003-4258-1483
authors.initials: S
authors.lastname: Lavandero
authors.affiliation: Laboratory of Cellular Communication, Advanced Center for Chronic Diseases (ACCDiS) and Center for Molecular Studies of the Cell, Program in Cell and Molecular Biology, Biomedical Sciences Institute (ICBM), Faculty of Medicine, University of Chile, 8380492 Santiago, Chile.
authors.forename: Andrew F G
authors.initials: AF
authors.lastname: Quest
mesh_terms: D000818:Animals; D001343:Autophagy; D006801:Humans; D008954:Models, Biological; D009369:Neoplasms / Q000473:pathology* / Q000503:physiopathology*; D025521:Tumor Suppressor Proteins / Q000378:metabolism*
chemical_list: D025521:Tumor Suppressor Proteins