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TET1 is a tumor suppressor of hematopoietic malignancy
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Journal Article
TET1 is a tumor suppressor of hematopoietic malignancy
2015
Overview
Methylation of DNA CpG motifs is modulated in part by the TET family of epigenetic regulators. Aifantis and colleagues show that loss of TET1 function biases hematopoiesis toward the B cell lineage and promotes hematopoietic malignancies.
The methylcytosine dioxygenase TET1 (‘ten-eleven translocation 1’) is an important regulator of 5-hydroxymethylcytosine (5hmC) in embryonic stem cells. The diminished expression of TET proteins and loss of 5hmC in many tumors suggests a critical role for the maintenance of this epigenetic modification. Here we found that deletion of
Tet1
promoted the development of B cell lymphoma in mice. TET1 was required for maintenance of the normal abundance and distribution of 5hmC, which prevented hypermethylation of DNA, and for regulation of the B cell lineage and of genes encoding molecules involved in chromosome maintenance and DNA repair. Whole-exome sequencing of TET1-deficient tumors revealed mutations frequently found in non-Hodgkin B cell lymphoma (B-NHL), in which
TET1
was hypermethylated and transcriptionally silenced. Our findings provide
in vivo
evidence of a function for TET1 as a tumor suppressor of hematopoietic malignancy.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
/ 13/31
/ 45
/ 45/100
/ 45/23
/ 45/91
/ 5-Methylcytosine - analogs & derivatives
/ 64
/ 64/60
/ Animals
/ Cell Differentiation - genetics
/ Cytosine - analogs & derivatives
/ DNA
/ DNA-Binding Proteins - genetics
/ DNA-Binding Proteins - metabolism
/ Embryonic Stem Cells - physiology
/ Hematopoietic stem cell disorders
/ Humans
/ Lymphoma
/ Mice
/ Proto-Oncogene Proteins - genetics
/ Proto-Oncogene Proteins - metabolism
/ Tumor Suppressor Proteins - genetics
/ Tumor Suppressor Proteins - metabolism
/ Tumors
