ArticleCancer research2017
Breast Cancer Suppression by Progesterone Receptors Is Mediated by Their Modulation of Estrogen Receptors and RNA Polymerase III.
Article in Cancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
42 citing papers in PubMed, 72 citations in OpenAlex.
- Nucleic sexual hormone receptor signaling pathways in breast cancer: function regulation, crosstalk, and therapeutic implications.NPJ precision oncology · 2026Review
- Brain FGF2 and NCAM1 contribute to FGFR1-dependent progression of estrogen receptor-positive breast cancer brain metastases.Nature communications · 2026Article
- Biomarkers in Spinal Metastasis of Breast Cancer: Insights Into Survival and Functional Outcomes.Journal of clinical neurology (Seoul, Korea) · 2026Article
- Evaluation of targeted and immune combination therapies in a rat model of hormone receptor-positive breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- PR inhibition stimulates G6PD expression to enhance malignancy in luminal breast cancer.Cell death & disease · 2025Article
- Maf1 cooperates with progesterone receptor to repress RNA polymerase III transcription of select tRNAs.Nucleic acids research · 2025Article
- Breaking Barriers in Breast Cancer: Multi-Targeted Therapeutic Insights.Mini reviews in medicinal chemistry · 2025Review
- Mechanistic analysis of enhancer sequences in the estrogen receptor transcriptional program.Communications biology · 2024Article
- Insulin-like growth factor binding protein-6 modulates proliferative antagonism in response to progesterone in breast cancer.Frontiers in endocrinology · 2024Article
- Molecular characterization of breast cancer cell pools with normal or reduced ability to respond to progesterone: a study based on RNA-seq.Journal, genetic engineering & biotechnology · 2023Article
- Selection of tRNA Genes in Human Breast Tumours Varies Substantially between Individuals.Cancers · 2023Article
- The recent progress of endocrine therapy-induced osteoporosis in estrogen-positive breast cancer therapy.Frontiers in oncology · 2023Review
- Targeting nuclear hormone receptors for the prevention of breast cancer.Frontiers in medicine · 2023Review
- Estrogen regulates divergent transcriptional and epigenetic cell states in breast cancer.Nucleic acids research · 2022Article
- Estrogen receptor positive breast cancers have patient specific hormone sensitivities and rely on progesterone receptor.Nature communications · 2022Article
- Widespread association of ERα with RMRP and tRNA genes in MCF-7 cells and breast cancers.Gene · 2022Article
- The Divergent Effects of Ovarian Steroid Hormones in the MCF-7 Model for Luminal A Breast Cancer: Mechanistic Leads for Therapy.International journal of molecular sciences · 2022Review
- Article
- Upregulation of an estrogen receptor-regulated gene by first generation progestins requires both the progesterone receptor and estrogen receptor alpha.Frontiers in endocrinology · 2022Article
- The Role of Progesterone Receptors in Breast Cancer.Drug design, development and therapy · 2022Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Greater than 50% of estrogen receptor (ER)-positive breast cancers coexpress the progesterone receptor (PR), which can directly and globally modify ER action to attenuate tumor growth. However, whether this attenuation is mediated only through PR-ER interaction remains unknown. To address this question, we assessed tumor growth in ER/PR-positive patient-derived xenograft models of breast cancer, where both natural and synthetic progestins were found to antagonize the mitogenic effects of estrogens. Probing the genome-wide mechanisms by which this occurs, we documented that chronic progestin treatment blunted ER-mediated gene expression up to 2-fold at the level of mRNA transcripts. Unexpectedly, <25% of all ER DNA binding events were affected by the same treatment. The PR cistrome displayed a bimodal distribution. In one group, >50% of PR binding sites were co-occupied by ER, with a propensity for both receptors to coordinately gain or lose binding in the presence of progesterone. In the second group, PR but not ER was associated with a large fraction of RNA polymerase III-transcribed tRNA genes, independent of hormone treatment. Notably, we discovered that PR physically associated with the Pol III holoenzyme. Select pre-tRNAs and mature tRNAs with PR and POLR3A colocalized at their promoters were relatively decreased in estrogen + progestin-treated tumors. Our results illuminate how PR may indirectly impede ER action by reducing the bioavailability of translational molecules needed for tumor growth.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.