| Literature DB >> 24862259 |
Juliet Goldsmith1, Beth Levine2, Jayanta Debnath3.
Abstract
The metabolism of malignant cells is profoundly altered in order to maintain their survival and proliferation in adverse microenvironmental conditions. Autophagy is an intracellular recycling process that maintains basal levels of metabolites and biosynthetic intermediates under starvation or other forms of stress, hence serving as an important mechanism for metabolic adaptation in cancer cells. Although it is widely acknowledged that autophagy sustains metabolism in neoplastic cells under duress, many questions remain with regard to the mutual relationship between autophagy and metabolism in cancer. Importantly, autophagy has often been described as a "double-edged sword" that can either impede or promote cancer initiation and progression. Here, we overview such a dual function of autophagy in tumorigenesis and our current understanding of the coordinated regulation of autophagy and cancer cell metabolism in the control of tumor growth, progression, and resistance to therapy.Entities:
Keywords: Autophagy; Cancer metabolism; Cancer therapy; Glutaminolysis; Glycolysis; Hypoxia
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Year: 2014 PMID: 24862259 PMCID: PMC5839656 DOI: 10.1016/B978-0-12-416618-9.00002-9
Source DB: PubMed Journal: Methods Enzymol ISSN: 0076-6879 Impact factor: 1.600