Cited by 175Estrogen and related hormone effectsBreast Cancer Treatment StudiesCancer-related Molecular Pathways

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Progestins both stimulate and inhibit breast cancer cell cycle progression while increasing expression of transforming growth factor alpha, epidermal growth factor receptor, c-fos, and c-myc genes.

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Musgrove, E A, Lee, C S, Sutherland, R L·1991·Molecular and Cellular Biology

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Abstract

This study documents a biphasic change in the rate of cell cycle progression and proliferation of T-47D human breast cancer cells treated with synthetic progestins, consisting of an initial transient acceleration in transit through G1, followed by cell cycle arrest and growth inhibition. Both components of the response were mediated via the progesterone receptor. The data are consistent with a model in which the action of progestins is to accelerate cells already progressing through G1, which are then arrested early in G1 after completing a round of replication, as are cells initially in other phases of the cell cycle. Such acceleration implies that progestins act on genes or gene products which are rate limiting for cell cycle progression. Increased production of epidermal growth factor and transforming growth factor alpha, putative autocrine growth factors in breast cancer cells, does not appear to account for the initial response to progestins, since although the mRNA abundance for these growth factors is rapidly induced by progestins, cells treated with epidermal growth factor or transforming growth factor alpha did not enter S phase until 5 to 6 h later than those stimulated by progestin. The proto-oncogenes c-fos and c-myc were rapidly but transiently induced by progestin treatment, paralleling the well-known response of these genes to mitogenic signals in other cell types. The progestin antagonist RU 486 inhibited progestin regulation of both cell cycle progression and c-myc expression, suggesting that this proto-oncogene may participate in growth modulation by progestins.

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Self-citation
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Authors: Musgrove, E. A., Lee, C. S., & Sutherland, R. L.
ORCID: Sutherland, R L
Venue: Molecular and Cellular Biology
Publisher: Informa UK Limited
Published: 1991-10
Volume: 11
Issue: 10
Pages: 5032-5043
ISSN: 0270-7306 (ISSN-L)
1098-5549
DOI: 10.1128/mcb.11.10.5032
OpenAlex: W4241665805
Cited by: 175
References: 0
Citations by year: 2025: 2 · 2023: 1 · 2022: 2 · 2020: 3 · 2019: 1 · 2018: 6 · 2017: 3 · 2016: 5 · 2015: 2 · 2014: 3 · 2013: 5 · 2012: 8
FWCI: 2.09
Type: journal article
Language: en
Open access: green
europepmc.org
Locations: Molecular and Cellular Biology (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
Funders: National Health and Medical Research Council
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Estrogen and related hormone effects
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Breast Cancer Treatment Studies
Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Keywords: progestins, breast cancer, cell cycle progression, progesterone receptor, T47D cells, G1 phase, cell cycle arrest, growth inhibition, transforming growth factor-alpha, epidermal growth factor receptor, c-fos, c-Myc, proto-oncogenes, autocrine growth factor, RU486, gene expression regulation

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Progestins both stimulate and inhibit breast cancer cell cycle progression while increasing expression of transforming growth factor alpha, epidermal growth factor receptor, c-fos, and c-myc genes.

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