Tumor Suppression and Promotion by Autophagy

التفاصيل البيبلوغرافية
العنوان: Tumor Suppression and Promotion by Autophagy
المؤلفون: Jimena Canales, Yenniffer Ávalos, Alfredo Criollo, Sergio Lavandero, Roberto Bravo-Sagua, Andrew F. G. Quest
المصدر: BioMed Research International
BioMed Research International, Vol 2014 (2014)
بيانات النشر: Hindawi Limited, 2014.
سنة النشر: 2014
مصطلحات موضوعية: Programmed cell death, General Immunology and Microbiology, biology, Tumor Suppressor Proteins, lcsh:R, Autophagy, lcsh:Medicine, Cellular homeostasis, Review Article, General Medicine, medicine.disease_cause, Models, Biological, General Biochemistry, Genetics and Molecular Biology, Cell biology, Neoplasms, biology.protein, medicine, Animals, Humans, PTEN, Carcinogenesis, Protein kinase B, PI3K/AKT/mTOR pathway, RHEB
الوصف: 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.
تدمد: 2314-6141
2314-6133
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::69bf7aa3270d49f87be44714c9d889acTest
https://doi.org/10.1155/2014/603980Test
حقوق: OPEN
رقم الانضمام: edsair.doi.dedup.....69bf7aa3270d49f87be44714c9d889ac
قاعدة البيانات: OpenAIRE