O-GlcNAc signaling in cancer metabolism and epigenetics.
The covalent attachment of β-D-N-acetylglucosamine monosaccharides (O-GlcNAc) to serine/threonine residues of nuclear and cytoplasmic proteins is a major regulatory mechanism in cell physiology. Aberrant O-GlcNAc modification of signaling proteins, metabolic enzymes, and transcriptional and epigenetic regulators has been implicated in cancer. Relentless growth of cancer cells requires metabolic reprogramming that is intertwined with changes in the epigenetic landscape. This review highlights the emerging role of protein O-GlcNAcylation at the interface of cancer metabolism and epigenetics.
Program in Integrative Cell Signaling and Neurobiology of Metabolism, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06519, USA; Section of Comparative Medicine, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06519, USA.
Jay Prakash
JP
Singh
Program in Integrative Cell Signaling and Neurobiology of Metabolism, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06519, USA; Section of Comparative Medicine, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06519, USA; Department of Cellular & Molecular Physiology, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06519, USA.
Kaisi
K
Zhang
Program in Integrative Cell Signaling and Neurobiology of Metabolism, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06519, USA; Section of Comparative Medicine, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06519, USA; School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi 710049, China.
Jing
J
Wu
Program in Integrative Cell Signaling and Neurobiology of Metabolism, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06519, USA; Section of Comparative Medicine, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06519, USA; Department of Cellular & Molecular Physiology, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06519, USA. Electronic address: xiaoyong.yang@yale.edu.
Xiaoyong
X
Yang
D000117:Acetylglucosamine / Q000378:metabolism*; D000951:Antigens, Neoplasm / Q000378:metabolism; D049109:Cell Proliferation; D004734:Energy Metabolism / Q000235:genetics*; D044127:Epigenesis, Genetic; D006031:Glycosylation; D051548:Histone Acetyltransferases / Q000378:metabolism; D006657:Histones / Q000378:metabolism; D006801:Humans; D006821:Hyaluronoglucosaminidase / Q000378:metabolism; D017351:N-Acetylglucosaminyltransferases / Q000378:metabolism; D009369:Neoplasms / Q000235:genetics* / Q000378:metabolism*; D011499:Protein Processing, Post-Translational / Q000502:physiology*; D012694:Serine / Q000378:metabolism; D015398:Signal Transduction / Q000235:genetics; D013912:Threonine / Q000378:metabolism; D014157:Transcription Factors / Q000378:metabolism; D014158:Transcription, Genetic / Q000235:genetics; D015533:Transcriptional Activation
D000951:Antigens, Neoplasm; D006657:Histones; D014157:Transcription Factors; D013912:Threonine; D012694:Serine; D051548:Histone Acetyltransferases; D017351:N-Acetylglucosaminyltransferases; C063057:UDP-N-acetylglucosamine-peptide beta-N-acetylglucosaminyltransferase; C115866:OGA protein, human; D006821:Hyaluronoglucosaminidase; D000117:Acetylglucosamine
Cancer metabolism; Epigenetics; O-GlcNAc; Posttranslational modifications