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Monoacylglycerol Lipase Regulates a Fatty Acid Network that Promotes Cancer Pathogenesis
Open accessAbstract
Tumor cells display progressive changes in metabolism that correlate with malignancy, including development of a lipogenic phenotype. How stored fats are liberated and remodeled to support cancer pathogenesis, however, remains unknown. Here, we show that the enzyme monoacylglycerol lipase (MAGL) is highly expressed in aggressive human cancer cells and primary tumors, where it regulates a fatty acid network enriched in oncogenic signaling lipids that promotes migration, invasion, survival, and in vivo tumor growth. Overexpression of MAGL in nonaggressive cancer cells recapitulates this fatty acid network and increases their pathogenicity-phenotypes that are reversed by an MAGL inhibitor. Impairments in MAGL-dependent tumor growth are rescued by a high-fat diet, indicating that exogenous sources of fatty acids can contribute to malignancy in cancers lacking MAGL activity. Together, these findings reveal how cancer cells can co-opt a lipolytic enzyme to translate their lipogenic state into an array of protumorigenic signals. PAPERFLICK:
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“An elevated expression of lipoprotein lipase (LPL) and monoacylglycerol lipase (MAGL) across diverse cancer subtypes and correlates with invasiveness”
From The emerging hallmarks of cancer metabolism (2016) · cites this paper as Nomura et al., 2010
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Metadata
- Authors
- Nomura, D. K., Long, J. Z., Niessen, S., Hoover, H. S., Ng, S.-W., & Cravatt, B. F.
- Affiliations
- Scripps Research Institute (US)
- Brigham and Women's Hospital (US)
- Corresponding author
- Cravatt, Benjamin F.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2010-01
- Volume
- 140
- Issue
- 1
- Pages
- 49-61
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC2885975
- OpenAlex
- W2127624416
- Cited by
- 1,002
- References
- 69
- Citations by year
- 2026: 40 · 2025: 41 · 2024: 55 · 2023: 46 · 2022: 59 · 2021: 78 · 2020: 69 · 2019: 67 · 2018: 69 · 2017: 60 · 2016: 75 · 2015: 72 · 2014: 70 · 2013: 61 · 2012: 47
- FWCI
- 15.66
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 1293 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute (R01CA132630, CA-087660, R37CA087660, R01CA087660, CA132630)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Sphingolipid Metabolism and Signaling
- Keywords
- monoacylglycerol lipase, fatty acid metabolism, lipolysis, tumor cell migration and invasion, tumor growth, MAGL inhibitors, high-fat diet, cancer metabolism
- MeSH terms
- Animals, Cell Line, Fatty Acids, Female, Humans, Monoacylglycerol Lipases, Neoplasm Transplantation, Ovarian Neoplasms, Transplantation, Heterologous, Tumor Cells, Cultured, Monoglycerides, Mice
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