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Auto-regulation of the estrogen receptor promoter
Abstract
The presence or absence of estrogen receptor (ER) plays a key role in the diagnosis and treatment of breast tumors. It is known that patients with breast tumors classified as ER-positive have a better prognosis. Observations such as this have led us to explore the question of what makes some breast tumors overexpress ER whereas others express either very low levels or none at all. To begin a study of ER regulation, we first chose to examine a 200 bp region of the ER promoter located immediately upstream from the transcribed sequence of the human ER gene. We found that this region of the ER promoter contained basal activity when transiently transfected into ER-negative HeLa cells. ER promoter activity was further increased by co-transfection of a wild-type ER expression vector, and this increased activity was hormone-dependent. Several ER deletion mutant constructs were also able to increase the activity of the ER promoter fragment, but none could support equivalent activity as was seen with the full-length ER. Therefore, we conclude that the ER can contribute to its own expression, and we hypothesize that this auto-regulation may contribute to its overexpression in some breast tumors.
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Estrogen receptors (especially ERβ) often regulate themselves in an autocrine manner; thus, higher estrogen levels may increase receptor synthesis through positive feedback.
“Estrogen receptors (especially ERβ) often regulate themselves in an autocrine manner; thus, higher estrogen levels may increase receptor synthesis through positive feedback [52].”
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“Estrogen receptors (especially ER β ) often regulate themselves in an autocrine manner; thus, higher estrogen levels may increase receptor synthesis through positive feedback [52].”
Metadata
- Authors
- Castles, C. G., Oesterreich, S., Hansen, R., & Fuqua, S. A. W.
- Affiliations
- The University of Texas at San Antonio Health Science Center (US)
- Corresponding author
- Fuqua, S.A.W.
- Venue
- The Journal of Steroid Biochemistry and Molecular Biology
- Publisher
- Elsevier BV
- Published
- 1997-06
- Volume
- 62
- Issue
- 2-3
- Pages
- 155-163
- ISSN
- 0960-0760 (ISSN-L)
- OpenAlex
- W2033436442
- Cited by
- 80
- References
- 42
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 1 · 2023: 1 · 2022: 2 · 2021: 4 · 2020: 1 · 2019: 1 · 2018: 2 · 2017: 2 · 2016: 3 · 2015: 6 · 2014: 1 · 2013: 4 · 2012: 5
- FWCI
- 1.13
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Journal of Steroid Biochemistry and Molecular Biology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Cancer Institute (P30CA 54174, P30CA054174, P01CA030195, CA-30195)
- 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
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Keywords
- estrogen receptor, breast tumors, estrogen receptor-positive breast cancer, hormone-dependent transcription, HeLa cells
- MeSH terms
- Gene Expression Regulation, HeLa Cells, Humans, Promoter Regions, Genetic, Receptors, Estrogen, Transfection, Autocrine Communication
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