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Metabolic Interactions with Cancer Epigenetics

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Journal Mol Aspects Med
Date 2016 Sep 14
PMID 27620316
Citations 30
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Abstract

Cancer cells have epigenetic alterations that are known to drive cancer progression. The reversibility of the epigenetic posttranslational modifications on chromatin and DNA renders targeting these modifications an attractive means for cancer therapy. Cellular epigenetic status interacts with cell metabolism, and we are now beginning to understand the nature of how this interaction occurs and the biological contexts that mediate its function. Given the tremendous interest in understanding and targeting metabolic reprogramming in cancer, this nexus also provides opportunities for exploring the liabilities of cancers. This review summarizes recent developments in our understanding of the interaction of cancer metabolism and epigenetics.

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References
1.
Shimazu T, Hirschey M, Newman J, He W, Shirakawa K, Le Moan N . Suppression of oxidative stress by β-hydroxybutyrate, an endogenous histone deacetylase inhibitor. Science. 2012; 339(6116):211-4. PMC: 3735349. DOI: 10.1126/science.1227166. View

2.
Lee J, Carrer A, Shah S, Snyder N, Wei S, Venneti S . Akt-dependent metabolic reprogramming regulates tumor cell histone acetylation. Cell Metab. 2014; 20(2):306-319. PMC: 4151270. DOI: 10.1016/j.cmet.2014.06.004. View

3.
Morgan H, Santos F, Green K, Dean W, Reik W . Epigenetic reprogramming in mammals. Hum Mol Genet. 2005; 14 Spec No 1:R47-58. DOI: 10.1093/hmg/ddi114. View

4.
Dang L, Jin S, Su S . IDH mutations in glioma and acute myeloid leukemia. Trends Mol Med. 2010; 16(9):387-97. DOI: 10.1016/j.molmed.2010.07.002. View

5.
Schug Z, Peck B, Jones D, Zhang Q, Grosskurth S, Alam I . Acetyl-CoA synthetase 2 promotes acetate utilization and maintains cancer cell growth under metabolic stress. Cancer Cell. 2015; 27(1):57-71. PMC: 4297291. DOI: 10.1016/j.ccell.2014.12.002. View