|
|
 Previous Article | Table of Contents | Next Article 
Activation of apoptosis associated with enforced myc expression in myeloid
progenitor cells is dominant to the suppression of apoptosis by
interleukin-3 or erythropoietin
DS Askew, JN Ihle and JL Cleveland
Department of Biochemistry, St Jude Children's Research Hospital, Memphis,
TN 38105.
The inappropriate expression of c-myc in cells deprived of growth factors
has recently been implicated in the activation of programmed cell death
(apoptosis). The studies described here examine the ability of
interleukin-3 (IL-3) or erythropoietin (Epo) to suppress apoptosis that
occurs in association with enforced myc expression during cell cycle arrest
of a murine IL-3-dependent myeloid progenitor cell line, 32D. G1 arrest was
observed when culturing 32D cells to high density in medium supplemented
with IL-3, or at subconfluent densities in medium supplemented with Epo.
Under both conditions, endogenous c-myc expression was downregulated and
viability was maintained. In clones of cells in which c-myc is
constitutively expressed from a retroviral vector, enforced c-myc
expression was associated with the activation of apoptosis at high cell
densities. Similarly, enforced c-myc expression was deleterious to cell
survival when these cells were cultured in Epo, as apoptosis was evident
within 6 hours. The results support the concept that inappropriate c-myc
expression activates apoptosis and that neither IL-3 nor Epo can suppress
this program under these conditions.
Volume 82,
Issue 7,
pp. 2079-2087,
10/01/1993
Copyright © 1993 by The American Society of Hematology
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
A. Hashimoto, K. Hirose, and M. Iino
BAD Detects Coincidence of G2/M Phase and Growth Factor Deprivation to Regulate Apoptosis
J. Biol. Chem.,
July 15, 2005;
280(28):
26225 - 26232.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
G.I. EVAN, M. CHRISTOPHOROU, E.A. LAWLOR, I. RINGSHAUSEN, J. PRESCOTT, T. DANSEN, A. FINCH, C. MARTINS, and D. MURPHY
Oncogene-dependent Tumor Suppression: Using the Dark Side of the Force for Cancer Therapy
Cold Spring Harb Symp Quant Biol,
January 1, 2005;
70(0):
263 - 273.
[Abstract]
[PDF]
|
|
|
|
|
|
|
M. S. Boosalis, R. Bandyopadhyay, E. H. Bresnick, B. S. Pace, K. Van DeMark, B. Zhang, D. V. Faller, and S. P. Perrine
Short-chain fatty acid derivatives stimulate cell proliferation and induce STAT-5 activation
Blood,
May 15, 2001;
97(10):
3259 - 3267.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C. E. Nesbit, S. Fan, H. Zhang, and E. V. Prochownik
Distinct Apoptotic Responses Imparted by c-myc and max
Blood,
August 1, 1998;
92(3):
1003 - 1010.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
H. Zhang, S. Fan, and E. V. Prochownik
Distinct Roles for MAX Protein Isoforms in Proliferation and Apoptosis
J. Biol. Chem.,
July 11, 1997;
272(28):
17416 - 17424.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S G Kennedy, A J Wagner, S D Conzen, J Jordan, A Bellacosa, P N Tsichlis, and N Hay
The PI 3-kinase/Akt signaling pathway delivers an anti-apoptotic signal.
Genes & Dev.,
March 15, 1997;
11(6):
701 - 713.
[Abstract]
[PDF]
|
|
|
|
|
|
|
H. Zhuang, Z. Niu, T.-C. He, S. V. Patel, and D. M. Wojchowski
Erythropoietin-dependent Inhibition of Apoptosis Is Supported by Carboxyl-truncated Receptor Forms and Blocked by Dominant-negative Forms of Jak2
J. Biol. Chem.,
June 16, 1995;
270(24):
14500 - 14504.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
