Inhibitory Effect of Estrogens on GCDFP-15 mRNA Levels and Secretion in ZR-75-1 Human Breast Cancer Cells
Abstract
In order to better understand the mechanisms responsible for the antagonism between steroids in human breast cancer cells, we have studied the effect of 17 beta-estradiol (E2), dihydrotestosterone (DHT), and dexamethasone (DEX) alone or in combination on the expression of the breast gross cystic disease fluid protein-15 (GCDFP-15) in ZR-75-1 cells. Incubation with E2 markedly decreased basal GCDFP-15 mRNA levels accompanied by a parallel inhibition of the secretion of this tumor marker, the estrogenic effect being exerted at a half-maximal concentration of about 44 pM E2. The inhibitory effect of E2 on GCDFP-15 expression was competitively reversed by the antiestrogen LY156758. In addition, 1 nM E2 inhibited the marked stimulation induced by 1 nM DHT or 300 nM DEX on GCDFP-15 mRNA accumulation and on the secretion of the glycoprotein. However, at the concentration used, E2 reversed by only 65% the stimulation achieved by the combination of DHT and DEX on GCDFP-15 mRNA levels. It is of interest to mention that the effect of DHT, DEX, and E2 on GCDFP-15 expression is opposite to the respective effect of each steroid on ZR-75-1 cell proliferation. The present data on the regulation of GCDFP-15 mRNA demonstrate an estrogen-induced inhibition of mRNA levels under physiological conditions, thus offering a unique opportunity to study the mechanisms involved in the down-regulation of gene expression by estrogens and to achieve a better understanding of the antagonism between estrogens, androgens, glucocorticoids, and progestins in breast cancer cells. Furthermore, GCDFP-15 could well be a good marker for monitoring the response to androgens and antiestrogens during the course of breast cancer therapy.
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Our previous studies have clearly demonstrated that androgens exert a direct inhibitory effect on the proliferation of human breast cancer cells.
“our previous studies have clearly demonstrated that androgens exert a direct inhibitory effect on the proliferation of human breast cancer cells (208 -213).”
From Endocrine and intracrine sources of androgens in women: inhibition of breast cancer and other roles of androgens and their precursor dehydroepiandrosterone (2003) · cites this paper as [211]
The effect of androgens on ZR-75-1 cell proliferation cannot be solely explained by the suppression of ER expression, because androgens still exert very potent inhibitory effects on growth in the absence of estrogens, even after prolonged periods of estrogen deprivation before exposure to androgens.
“The effect of androgens on ZR-75-1 cell proliferation, however, cannot be solely explained by the suppression of ER expression, because androgens still exert very potent inhibitory effects on growth in the absence of estrogens, even after prolonged periods of estrogen deprivation before exposure to androgens (208,211).”
From Endocrine and intracrine sources of androgens in women: inhibition of breast cancer and other roles of androgens and their precursor dehydroepiandrosterone (2003) · cites this paper as [211]
The data summarized above clearly support the hypothesis that at least part of the antagonism observed between the action of androgens and estrogens in breast cancer cells may be explained by the heterologous downregulation of the ER by an AR-mediated mechanism.
“The data summarized above clearly support the hypothesis that at least part of the antagonism observed between the action of androgens and estrogens in breast cancer cells (208,211,215,240) may be explained by the heterologous downregulation of the ER by an AR-mediated mechanism.”
From Endocrine and intracrine sources of androgens in women: inhibition of breast cancer and other roles of androgens and their precursor dehydroepiandrosterone (2003) · cites this paper as [211]
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Self-citation
- Authors
- Simard, J., Hatton, A. C., Labrief, C., Dauvois, S., Zhao, H. F., Haagensen, D. E., & Labrie, F.
- Affiliations
- Université Laval (CA)
- Venue
- Molecular Endocrinology
- Publisher
- The Endocrine Society
- Published
- 1989-04
- Volume
- 3
- Issue
- 4
- Pages
- 694-702
- ISSN
- 0888-8809 (ISSN-L)
- 1944-9917
- OpenAlex
- W2021149804
- Cited by
- 72
- References
- 27
- Citations by year
- 2023: 1 · 2022: 1 · 2021: 15 · 2020: 1 · 2019: 2 · 2018: 2 · 2016: 2 · 2013: 1
- FWCI
- 3.01
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Molecular Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Breast Cancer Treatment Studies
- Health Sciences › Medicine › Pathology and Forensic Medicine › Breast Lesions and Carcinomas
- Keywords
- GCDFP-15, breast cancer, ZR-75-1 cells, estradiol, dihydrotestosterone, dexamethasone, estrogen antagonism, gene expression regulation, androgen antagonism, glucocorticoid antagonism, cell proliferation
- MeSH terms
- Apolipoproteins, Breast Neoplasms, Carrier Proteins, Cell Division, Dexamethasone, Estradiol, Estrogen Antagonists, Estrogens, Female, Gene Expression Regulation, Glycoproteins, Humans, Neoplasm Proteins, Piperidines, RNA, Messenger, Dihydrotestosterone, Blotting, Northern, DNA Probes, Raloxifene Hydrochloride, Membrane Transport Proteins, Apolipoproteins D
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