Inhibition of TET2-mediated conversion of 5-methylcytosine to 5-hydroxymethylcytosine disturbs erythroid and granulomonocytic differentiation of human hematopoietic progenitors

Blood. 2011 Sep 1;118(9):2551-5. doi: 10.1182/blood-2010-12-324707. Epub 2011 Jul 6.

Abstract

TET2 converts 5-methylcytosine to 5-hydroxymethylcytosine (5-hmC) in DNA and is frequently mutated in myeloid malignancies, including myeloproliferative neoplasms. Here we show that the level of 5-hmC is decreased in granulocyte DNA from myeloproliferative neoplasm patients with TET2 mutations compared with granulocyte DNA from healthy patients. Inhibition of TET2 by RNA interference decreases 5-hmC levels in both human leukemia cell lines and cord blood CD34(+) cells. These results confirm the enzymatic function of TET2 in human hematopoietic cells. Knockdown of TET2 in cord blood CD34(+) cells skews progenitor differentiation toward the granulomonocytic lineage at the expense of lymphoid and erythroid lineages. In addition, by monitoring in vitro granulomonocytic development we found a decreased granulocytic differentiation and an increase in monocytic cells. Our results indicate that TET2 disruption affects 5-hmC levels in human myeloid cells and participates in the pathogenesis of myeloid malignancies through the disturbance of myeloid differentiation.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • 5-Methylcytosine / metabolism*
  • Cell Line, Tumor
  • Cell Lineage
  • Colony-Forming Units Assay
  • Cytosine / analogs & derivatives*
  • Cytosine / biosynthesis
  • DNA Methylation / genetics*
  • DNA-Binding Proteins / antagonists & inhibitors
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / physiology*
  • Dioxygenases
  • Erythropoiesis / genetics*
  • Erythropoiesis / physiology
  • Fetal Blood / cytology
  • Genetic Vectors / genetics
  • Granulocytes / metabolism
  • Granulocytes / pathology
  • Hematopoietic Stem Cells / cytology*
  • Humans
  • Lentivirus / genetics
  • Monocytes / metabolism
  • Monocytes / pathology
  • Mutation
  • Myelopoiesis / genetics*
  • Myelopoiesis / physiology
  • Proto-Oncogene Proteins / antagonists & inhibitors
  • Proto-Oncogene Proteins / genetics
  • Proto-Oncogene Proteins / physiology*
  • RNA Interference*
  • RNA, Small Interfering / administration & dosage
  • RNA, Small Interfering / genetics*

Substances

  • DNA-Binding Proteins
  • Proto-Oncogene Proteins
  • RNA, Small Interfering
  • 5-hydroxymethylcytosine
  • 5-Methylcytosine
  • Cytosine
  • Dioxygenases
  • TET2 protein, human
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