TET-Mediated Hypermethylation Primes SDH-Deficient Cells for HIF2α-Driven Mesenchymal Transition.
5-Methylcytosine
/ analogs & derivatives
Adult
Aged
Animals
Basic Helix-Loop-Helix Transcription Factors
/ metabolism
Cell Hypoxia
Cell Line
Cell Line, Tumor
DNA Methylation
/ genetics
DNA-Binding Proteins
/ metabolism
Dioxygenases
Female
Gene Expression Regulation, Neoplastic
Gene Knockdown Techniques
Genome, Human
Humans
Male
Mesoderm
/ metabolism
Mice, Nude
Middle Aged
Mutation
/ genetics
Neoplasm Metastasis
Phenotype
Polycomb Repressive Complex 2
/ metabolism
Proto-Oncogene Proteins
/ metabolism
Succinate Dehydrogenase
/ deficiency
SDH
SDHB
epithelial-to-mesenchymal transition
hydroxymethylation
hypoxia
methylation
paraganglioma
pheochromocytoma
succinate dehydrogenase
Journal
Cell reports
ISSN: 2211-1247
Titre abrégé: Cell Rep
Pays: United States
ID NLM: 101573691
Informations de publication
Date de publication:
31 03 2020
31 03 2020
Historique:
received:
06
02
2019
revised:
24
01
2020
accepted:
06
03
2020
entrez:
3
4
2020
pubmed:
3
4
2020
medline:
27
3
2021
Statut:
ppublish
Résumé
Loss-of-function mutations in the SDHB subunit of succinate dehydrogenase predispose patients to aggressive tumors characterized by pseudohypoxic and hypermethylator phenotypes. The mechanisms leading to DNA hypermethylation and its contribution to SDH-deficient cancers remain undemonstrated. We examine the genome-wide distribution of 5-methylcytosine and 5-hydroxymethylcytosine and their correlation with RNA expression in SDHB-deficient tumors and murine Sdhb
Identifiants
pubmed: 32234487
pii: S2211-1247(20)30329-6
doi: 10.1016/j.celrep.2020.03.022
pii:
doi:
Substances chimiques
Basic Helix-Loop-Helix Transcription Factors
0
DNA-Binding Proteins
0
Proto-Oncogene Proteins
0
TET1 protein, mouse
0
5-hydroxymethylcytosine
1123-95-1
endothelial PAS domain-containing protein 1
1B37H0967P
5-Methylcytosine
6R795CQT4H
Dioxygenases
EC 1.13.11.-
Tet2 protein, mouse
EC 1.13.11.-
Succinate Dehydrogenase
EC 1.3.99.1
Polycomb Repressive Complex 2
EC 2.1.1.43
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
4551-4566.e7Informations de copyright
Copyright © 2020 The Author(s). Published by Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Interests The authors declare no competing interests.