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J. Biol. Chem., Vol. 276, Issue 24, 21464-21475, June 15, 2001
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From the By use of cDNA array technology we have
screened 588 genes to determine the effect of autocrine production of
human growth hormone (hGH) on gene expression in human mammary
carcinoma cells. We have used a previously described cellular model to
study autocrine hGH function in which the hGH gene or a
translation-deficient hGH gene was stably transfected into MCF-7 cells.
Fifty two of the screened genes were regulated, either positively (24)
or negatively (28), by autocrine production of hGH. We have now characterized the role of one of the up-regulated genes,
chop (gadd153), in the effect of autocrine
production of hGH on mammary carcinoma cell number. The effect of
autocrine production of hGH on the level of CHOP mRNA was exerted
at the transcriptional level as autocrine hGH increased chloramphenicol
acetyltransferase production from a reporter plasmid containing a
1-kilobase pair fragment of the chop promoter. The
autocrine hGH-stimulated increase in CHOP mRNA also resulted in an
increase in CHOP protein. As a consequence, autocrine hGH stimulation
of CHOP-mediated transcriptional activation was increased. Stable
transfection of human CHOP cDNA into mammary carcinoma cells
demonstrated that CHOP functioned not as a mediator of hGH-stimulated
mitogenesis but rather enhanced the protection from apoptosis afforded
by hGH in a p38 MAPK-dependent manner. Thus transcriptional
up-regulation of chop is one mechanism by which hGH
regulates mammary carcinoma cell number.
Autocrine Human Growth Hormone (hGH) Regulation of Human Mammary
Carcinoma Cell Gene Expression
IDENTIFICATION OF CHOP AS A MEDIATOR OF hGH-STIMULATED HUMAN
MAMMARY CARCINOMA CELL SURVIVAL*
§¶,§,,
,
Institute of Molecular and Cell Biology, 30 Medical Drive, Singapore 117609, Republic of Singapore, the
Department of Medicine, National University of Singapore,
Singapore 119074, Republic of Singapore, and ** CNRS UMR 5578, Physiologies Energetiques Cellulaires et Moléculaires,
Université Claude Bernard, Lyon-1, France
*
This work was supported by the National Science and
Technology Board of Singapore (to P. E. L.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Inst. of Molecular
and Cell Biology, 30 Medical Dr., Singapore 117609, Republic of
Singapore. Tel.: 65-8747847; Fax: 65-7791117; E-mail: mcbpel@ imcb.nus.edu.sg.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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