Roles and Regulations of TET Enzymes in Solid Tumors.

Abstract	The mechanisms governing the methylome profile of tumor suppressors and oncogenes have expanded with the discovery of oxidized states of 5-methylcytosine (5mC). Ten-eleven translocation (TET) enzymes are a family of dioxygenases that iteratively catalyze 5mC oxidation and promote cytosine demethylation, thereby creating a dynamic global and local methylation landscape. While the catalytic function of TET enzymes during stem cell differentiation and development have been well studied, less is known about the multifaceted roles of TET enzymes during carcinogenesis. This review outlines several tiers of TET regulation and overviews how TET deregulation promotes a cancer phenotype. Defining the tissue-specific and context-dependent roles of TET enzymes will deepen our understanding of the epigenetic perturbations that promote or inhibit carcinogenesis.
Authors	Julie K Bray, Meelad M Dawlaty, Amit Verma, Anirban Maitra
Journal	Trends in cancer (Trends Cancer) Vol. 7 Issue 7 Pg. 635-646 (07 2021) ISSN: 2405-8025 [Electronic] United States
PMID	33468438 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Review)
Copyright	Published by Elsevier Inc.
Chemical References	DNA-Binding Proteins Immune Checkpoint Inhibitors Proto-Oncogene Proteins 5-Methylcytosine Mixed Function Oxygenases TET1 protein, human TET3 protein, human Dioxygenases TET2 protein, human
Topics	5-Methylcytosine (metabolism) Antineoplastic Combined Chemotherapy Protocols (pharmacology, therapeutic use) Carcinogenesis (genetics, immunology, pathology) Clinical Trials as Topic DNA Methylation (drug effects, immunology) DNA-Binding Proteins (antagonists & inhibitors, genetics, metabolism) Dioxygenases (antagonists & inhibitors, genetics, metabolism) Drug Synergism Epigenesis, Genetic (drug effects, immunology) Gene Expression Regulation, Neoplastic (drug effects, immunology) Humans Immune Checkpoint Inhibitors (pharmacology, therapeutic use) Mixed Function Oxygenases (antagonists & inhibitors, genetics, metabolism) Mutation Neoplasms (drug therapy, genetics, immunology, pathology) Proto-Oncogene Proteins (antagonists & inhibitors, genetics, metabolism) Treatment Outcome

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