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J. Biol. Chem., Vol. 277, Issue 29, 26662-26672, July 19, 2002
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From the Multiple cellular effects of human growth hormone
(hGH) are mediated by an indirect mechanism requiring transcriptional
activation of genes encoding protein effector molecules such as
insulin-like growth factor-1. Such protein effector molecules then act
directly to mediate the cellular functions of hGH. We report here that autocrine hGH production by mammary carcinoma cells specifically results in the transcriptional repression of the p53-regulated placental transforming growth factor-
Autocrine Human Growth Hormone Inhibits Placental Transforming
Growth Factor-
Gene Transcription to Prevent Apoptosis and Allow
Cell Cycle Progression of Human Mammary Carcinoma Cells*
,,¶
Institute of Molecular and Cell Biology, 30 Medical Drive, Singapore 117609, the ¶ Department of Medicine,
National University of Singapore, Singapore 119074, Republic of Singapore, and § Cancer Molecular Sciences,
Pfizer Global Research and Development, Ann Arbor Laboratories,
Ann Arbor, Michigan 48105
(PTGF-) gene.
Transcriptional repression of the PTGF- gene does not
require the p53-binding sites in the PTGF- promoter, and
autocrine hGH also desensitized the response of the
PTGF- promoter to p53 overexpression. Transcriptional repression of the PTGF- gene is accompanied by
consequent decreases in its protein product, Smad-mediated
transcription, and its cellular effects that include cell cycle arrest
and apoptosis. PTGF- specifically inhibited the autocrine
hGH-stimulated expression of cyclin D1 required for autocrine
hGH-stimulated mammary carcinoma cell cycle progression. Thus, one
mechanism by which autocrine hGH promotes an increase in mammary
carcinoma cell number is by transcriptional repression of protein
effector molecules that promote cell cycle arrest and apoptosis. Such
transcriptional repression of negative regulatory factors, such as
PTGF-, may also be requisite for direct stimulation of mammary
carcinoma cell mitogenesis by hGH.
*
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: Institute of
Molecular and Cell Biology, 30 Medical Dr., Singapore 117609, Republic of Singapore. Tel.: 65-68747847; Fax: 65-67791117; E-mail:
mcbpel@imcb.nus.edu.sg.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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