@article{fd5ecadb7ec84b5a98e6ce5e83dbe557,
title = "Hypoxia, hypoxia-inducible gene 2 (HIG2)/HILPDA, and intracellular lipolysis in cancer",
abstract = "Tumor tissues are chronically exposed to hypoxia owing to aberrant vascularity. Hypoxia induces metabolic alterations in cancer, thereby promoting aggressive malignancy and metastasis. While previous efforts largely focused on adaptive responses in glucose and glutamine metabolism, recent studies have begun to yield important insight into the hypoxic regulation of lipid metabolic reprogramming in cancer. Emerging evidence points to lipid droplet (LD) accumulation as a hallmark of hypoxic cancer cells. One critical underlying mechanism involves the inhibition of adipose triglyceride lipase (ATGL)-mediated intracellular lipolysis by a small protein encoded by hypoxia-inducible gene 2 (HIG2), also known as hypoxia inducible lipid droplet associated (HILPDA). In this review we summarize and discuss recent key findings on hypoxia-dependent regulation of metabolic adaptations especially lipolysis in cancer. We also pose several questions and hypotheses pertaining to the metabolic impact of lipolytic regulation in cancer under hypoxia and during hypoxia-reoxygenation transition.",
keywords = "ATGL, Fatty acid, HIF, HIG2, HILPDA, Hypoxia, Hypoxia inducible gene 2, Hypoxia-inducible factor, Lipid droplet, Lipolysis, Oxygen",
author = "Davide Povero and Johnson, {Scott M.} and Jun Liu",
note = "Funding Information: This publication was supported by research grant from the U.S. National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases ( DK109096 to J.L.), post-doctoral funding to D.P. from the U.S. National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, Institutional National Research Service Award (T32) in Diabetes and Metabolism ( 5T32DK007352-37 ), as well as predoctoral funding to S.M.J. from the Mayo Foundation for Medical Education and Research . This publication was also supported by CTSA Grant Number UL1 TR002377 from the National Center for Advancing Translational Science (NCATS) . Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the NIH. Funding Information: This publication was supported by research grant from the U.S. National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases (DK109096 to J.L.), post-doctoral funding to D.P. from the U.S. National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, Institutional National Research Service Award (T32) in Diabetes and Metabolism (5T32DK007352-37), as well as predoctoral funding to S.M.J. from the Mayo Foundation for Medical Education and Research. This publication was also supported by CTSA Grant Number UL1 TR002377 from the National Center for Advancing Translational Science (NCATS). Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the NIH. Publisher Copyright: {\textcopyright} 2020 Elsevier B.V.",
year = "2020",
month = nov,
day = "28",
doi = "10.1016/j.canlet.2020.06.013",
language = "English (US)",
volume = "493",
pages = "71--79",
journal = "Cancer Letters",
issn = "0304-3835",
publisher = "Elsevier Ireland Ltd",
}