Metabolic interactions with cancer epigenetics.
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.
Department of Pharmacology and Cancer Biology, Duke Cancer Institute, Duke Molecular Physiology Institute, Duke University School of Medicine, Durham, NC 27710, USA.
Xia
X
Gao
Department of Cancer Biology, Beckman Research Institute of City of Hope Cancer Center, Duarte, CA 91010, USA.
Michael A
MA
Reid
Department of Cancer Biology, Beckman Research Institute of City of Hope Cancer Center, Duarte, CA 91010, USA.
Mei
M
Kong
Department of Pharmacology and Cancer Biology, Duke Cancer Institute, Duke Molecular Physiology Institute, Duke University School of Medicine, Durham, NC 27710, USA. Electronic address: Jason.Locasale@duke.edu.
Jason W
JW
Locasale
D000818:Animals; D019175:DNA Methylation; D044127:Epigenesis, Genetic; D006657:Histones / Q000378:metabolism; D006801:Humans; D055442:Metabolome; D008954:Models, Biological; D009369:Neoplasms / Q000235:genetics*
D006657:Histones
Acetyl-CoA; Methionine; One-carbon metabolism; S-Adenosyl methionine; Serine; α-Ketoglutarate