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Blood, 1 June 2004, Vol. 103, No. 11, pp. 4259-4267. Prepublished online as a Blood First Edition Paper on February 24, 2004; DOI 10.1182/blood-2002-09-2704. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-09-2704v1 103/11/4259    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Shafarenko, M. Articles by Hoffman, B. Search for Related Content PubMed PubMed Citation Articles by Shafarenko, M. Articles by Hoffman, B. Related Collections Hematopoiesis and Stem Cells Neoplasia Apoptosis Oncogenes and Tumor Suppressors Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Fos modulates myeloid cell survival and differentiation and partially abrogates the c-Myc block in terminal myeloid differentiation Marianna Shafarenko, Arshad Amanullah, Bernard Gregory, Dan A. Liebermann, and Barbara Hoffman From the Fels Institute for Cancer Research and Molecular Biology and the Department of Biochemistry, Temple University School of Medicine, Philadelphia, PA. Previously, we have shown that Fos/Jun transcription factor complexes function as positive modulators of myeloid differentiation. Fos, which is stably induced during normal myeloid differentiation, is not induced upon differentiation of M1 myeloblastic leukemia cells. Establishing M1 cells that express a -estradiol-conditional FosER chimera, we show that in the absence of the differentiation inducer interleukin-6 (IL-6), Fos expression in M1 myeloblasts promoted apoptotic cell death, entailing cytochrome c release and caspase-9 activation. In contrast, in the presence of IL-6, Fos-mediated apoptosis was abrogated, and Fos promoted terminal differentiation, increasing the sensitivity of M1 cells to be induced for differentiation by IL-6. Fos-mediated apoptosis was accelerated by deregulated c-Myc. Furthermore, restoring Fos expression in M1 partially abrogated the block imparted by deregulated c-Myc on the myeloid differentiation program, increased the sensitivity of the cells to be induced for differentiation, and curtailed their leukemic phenotype. These data provide evidence that Fos/Jun transcription factor complexes play a role in modulating both myeloid cell survival and differentiation and suggest that genetic lesions that alter Fos expression may cooperate with deregulated c-Myc in leukemogenesis. (Blood. 2004;103:4259-4267) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: W. Yuan, J. E. Payton, M. S. Holt, D. C. Link, M. A. Watson, J. F. DiPersio, and T. J. Ley Commonly dysregulated genes in murine APL cells Blood, February 1, 2007; 109(3): 961 - 970. [Abstract] [Full Text] [PDF] X. Wang and G. P. Studzinski The Requirement for and Changing Composition of the Activating Protein-1 Transcription Factor during Differentiation of Human Leukemia HL60 Cells Induced by 1,25-Dihydroxyvitamin D3. Cancer Res., April 15, 2006; 66(8): 4402 - 4409. [Abstract] [Full Text] [PDF] M. Shafarenko, D. A. Liebermann, and B. Hoffman Egr-1 abrogates the block imparted by c-Myc on terminal M1 myeloid differentiation Blood, August 1, 2005; 106(3): 871 - 878. [Abstract] [Full Text] [PDF]

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