TEL/ETV6 induces apoptosis in 32D cells through p53-dependent pathways

Biochem Biophys Res Commun. 2006 Aug 25;347(2):517-26. doi: 10.1016/j.bbrc.2006.06.127. Epub 2006 Jun 30.


TEL is an ETS family transcription factor that is critical for maintaining hematopoietic stem cells in adult bone marrow. To investigate the roles of TEL in myeloid proliferation and differentiation, we introduced TEL cDNA into mouse myeloid 32Dcl3 cells. Overexpression of TEL repressed interleukin-3-dependent proliferation through blocking cell cycle progression. Also, the presence of TEL triggered apoptosis through the mitochondrial intrinsic pathway on exposure to granulocyte colony-stimulating factor. We found an increase in p53 protein and its DNA binding in the TEL-overexpressing cells. Forced expression of TEL stimulated transcription via the p53-responsive element and increased the expression of cellular target genes for p53 such as cell cycle regulator p21 and apoptosis inducer Puma. Consistently, induction of apoptosis was delayed by pifithrin-alpha treatment and completely blocked by increased expression of Bcl-2 in the TEL-overexpressing cells. These data collectively suggest that TEL exerts a tumor suppressive function through augmenting the p53 pathway and facilitates normal development of myelopoiesis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Apoptosis / physiology*
  • Benzothiazoles
  • Blotting, Northern
  • Blotting, Western
  • Cell Line
  • Cell Proliferation / drug effects
  • Granulocyte Colony-Stimulating Factor / pharmacology
  • Humans
  • Interleukin-3 / pharmacology
  • Membrane Potentials / drug effects
  • Mitochondrial Membranes / drug effects
  • Mitochondrial Membranes / physiology
  • Mutation
  • Proto-Oncogene Proteins c-bcl-2 / genetics
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Proto-Oncogene Proteins c-ets / genetics
  • Proto-Oncogene Proteins c-ets / physiology*
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Repressor Proteins / genetics
  • Repressor Proteins / physiology*
  • Signal Transduction*
  • Thiazoles / pharmacology
  • Toluene / analogs & derivatives
  • Toluene / pharmacology
  • Transcription, Genetic / drug effects
  • Transfection
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism
  • Tumor Suppressor Protein p53 / physiology*


  • Benzothiazoles
  • ETS translocation variant 6 protein
  • Interleukin-3
  • Proto-Oncogene Proteins c-bcl-2
  • Proto-Oncogene Proteins c-ets
  • RNA, Messenger
  • Repressor Proteins
  • Thiazoles
  • Tumor Suppressor Protein p53
  • Granulocyte Colony-Stimulating Factor
  • Toluene
  • pifithrin