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

Abstract

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.

Authors:
 [1];  [1];  [1];  [1]
  1. Department of Hematology, Dokkyo Medical University School of Medicine, Tochigi 321-0293 (Japan)
Publication Date:
OSTI Identifier:
20854429
Resource Type:
Journal Article
Journal Name:
Biochemical and Biophysical Research Communications
Additional Journal Information:
Journal Volume: 347; Journal Issue: 2; Other Information: DOI: 10.1016/j.bbrc.2006.06.127; PII: S0006-291X(06)01450-1; Copyright (c) 2006 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; APOPTOSIS; BONE MARROW; CELL CYCLE; CELL PROLIFERATION; DNA; LEUKOCYTES; MICE; MITOCHONDRIA; MONOCLINIC LATTICES; NEOPLASMS; STEM CELLS; TRANSCRIPTION; TRANSCRIPTION FACTORS

Citation Formats

Yamagata, Tetsuya, Maki, Kazuhiro, Waga, Kazuo, and Mitani, Kinuko. TEL/ETV6 induces apoptosis in 32D cells through p53-dependent pathways. United States: N. p., 2006. Web. doi:10.1016/j.bbrc.2006.06.127.
Yamagata, Tetsuya, Maki, Kazuhiro, Waga, Kazuo, & Mitani, Kinuko. TEL/ETV6 induces apoptosis in 32D cells through p53-dependent pathways. United States. https://doi.org/10.1016/j.bbrc.2006.06.127
Yamagata, Tetsuya, Maki, Kazuhiro, Waga, Kazuo, and Mitani, Kinuko. 2006. "TEL/ETV6 induces apoptosis in 32D cells through p53-dependent pathways". United States. https://doi.org/10.1016/j.bbrc.2006.06.127.
@article{osti_20854429,
title = {TEL/ETV6 induces apoptosis in 32D cells through p53-dependent pathways},
author = {Yamagata, Tetsuya and Maki, Kazuhiro and Waga, Kazuo and Mitani, Kinuko},
abstractNote = {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.},
doi = {10.1016/j.bbrc.2006.06.127},
url = {https://www.osti.gov/biblio/20854429}, journal = {Biochemical and Biophysical Research Communications},
issn = {0006-291X},
number = 2,
volume = 347,
place = {United States},
year = {Fri Aug 25 00:00:00 EDT 2006},
month = {Fri Aug 25 00:00:00 EDT 2006}
}