PU.1 silencing leads to terminal differentiation of erythroleukemia cells

Atar, Orna; Levi, Ben-Zion

doi:10.1016/j.bbrc.2005.02.109

Title: PU.1 silencing leads to terminal differentiation of erythroleukemia cells

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Abstract

The transcription factor PU.1 plays a central role in development and differentiation of hematopoietic cells. Evidence from PU.1 knockout mice indicates a pivotal role for PU.1 in myeloid lineage and B-lymphocyte development. In addition, PU.1 is a key player in the development of Friend erythroleukemia disease, which is characterized by proliferation and differentiation arrest of proerythrocytes. To study the role of PU.1 in erythroleukemia, we have used murine erythroleukemia cells, isolated from Friend virus-infected mice. Expression of PU.1 small interfering RNA in these cells led to significant inhibition of PU.1 levels. This was accompanied by inhibition of proliferation and restoration in the ability of the proerythroblastic cells to produce hemoglobin, i.e., reversion of the leukemic phenotype. The data suggest that overexpression of PU.1 gene is the immediate cause for maintaining the leukemic phenotype of the disease by retaining the self-renewal capacity of transformed erythroblastic cells and by blocking the terminal differentiation program towards erythrocytes.

Authors:

Atar, Orna ^[1]; Levi, Ben-Zion ^[1]

Department of Biotechnology and Food Engineering, Technion-Israel Institute of Technology, Haifa 32000 (Israel)

Publication Date:: Fri Apr 22 00:00:00 EDT 2005

OSTI Identifier:: 20709151

Resource Type:: Journal Article

Journal Name:: Biochemical and Biophysical Research Communications

Additional Journal Information:: Journal Volume: 329; Journal Issue: 4; Other Information: DOI: 10.1016/j.bbrc.2005.02.109; PII: S0006-291X(05)00317-7; Copyright (c) 2005 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; BIOLOGICAL RECOVERY; CELL PROLIFERATION; DISEASES; ERYTHROCYTES; HEMOGLOBIN; INHIBITION; KNOCK-OUT REACTIONS; LEAD; LYMPHOCYTES; MICE; PHENOTYPE; RNA; TRANSCRIPTION FACTORS; VIRUSES

Citation Formats


                    Atar, Orna, and Levi, Ben-Zion. PU.1 silencing leads to terminal differentiation of erythroleukemia cells.  United States: N. p., 2005. 
        Web.  doi:10.1016/j.bbrc.2005.02.109.

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                    Atar, Orna, & Levi, Ben-Zion. PU.1 silencing leads to terminal differentiation of erythroleukemia cells.  United States.  https://doi.org/10.1016/j.bbrc.2005.02.109

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                    Atar, Orna, and Levi, Ben-Zion. 2005.  
        "PU.1 silencing leads to terminal differentiation of erythroleukemia cells".  United States.  https://doi.org/10.1016/j.bbrc.2005.02.109.

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@article{osti_20709151,

  title        = {PU.1 silencing leads to terminal differentiation of erythroleukemia cells},

  author       = {Atar, Orna and Levi, Ben-Zion},

  abstractNote = {The transcription factor PU.1 plays a central role in development and differentiation of hematopoietic cells. Evidence from PU.1 knockout mice indicates a pivotal role for PU.1 in myeloid lineage and B-lymphocyte development. In addition, PU.1 is a key player in the development of Friend erythroleukemia disease, which is characterized by proliferation and differentiation arrest of proerythrocytes. To study the role of PU.1 in erythroleukemia, we have used murine erythroleukemia cells, isolated from Friend virus-infected mice. Expression of PU.1 small interfering RNA in these cells led to significant inhibition of PU.1 levels. This was accompanied by inhibition of proliferation and restoration in the ability of the proerythroblastic cells to produce hemoglobin, i.e., reversion of the leukemic phenotype. The data suggest that overexpression of PU.1 gene is the immediate cause for maintaining the leukemic phenotype of the disease by retaining the self-renewal capacity of transformed erythroblastic cells and by blocking the terminal differentiation program towards erythrocytes.},

  doi          = {10.1016/j.bbrc.2005.02.109},

  url          = {https://www.osti.gov/biblio/20709151},
  journal      = {Biochemical and Biophysical Research Communications},

  issn         = {0006-291X},

  number       = 4,

  volume       = 329,

  place        = {United States},

  year         = {Fri Apr 22 00:00:00 EDT 2005},

  month        = {Fri Apr 22 00:00:00 EDT 2005}

}

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