ArticleMolecular endocrinology (Baltimore, Md.)2009
Mechanism of BRCA1-mediated inhibition of progesterone receptor transcriptional activity.
Article in Molecular endocrinology (Baltimore, Md.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Novel insights linking BRCA1-IRIS role in mammary gland development to formation of aggressive PABCs: the case for longer breastfeeding.American journal of cancer research · 2022Article
- Interferon-γ signaling is associated withNPJ precision oncology · 2019Article
- Molecular Signaling of Progesterone, Growth Hormone, Wnt, and HER in Mammary Glands of Dogs, Rodents, and Humans: New Treatment Target Identification.Frontiers in veterinary science · 2017Review
- Article
- BRCA1 regulates insulin-like growth factor 1 receptor levels in ovarian cancer.Oncology letters · 2014Article
- Glucocorticoid receptor repression mediated by BRCA1 inactivation in ovarian cancer.BMC cancer · 2014Article
- BRCA1 as a nicotinamide adenine dinucleotide (NAD)-dependent metabolic switch in ovarian cancer.Cell cycle (Georgetown, Tex.) · 2014Article
- Regulation of angiotensin II type 1 receptor expression in ovarian cancer: a potential role for BRCA1.Journal of ovarian research · 2013Article
- Effect of BRCA1 on epidermal growth factor receptor in ovarian cancer.Journal of experimental & clinical cancer research : CR · 2013Article
- Ubiquitin- and ubiquitin-like proteins-conjugating enzymes (E2s) in breast cancer.Molecular biology reports · 2013Article
- B-cell translocation gene 2 (BTG2) stimulates cellular antioxidant defenses through the antioxidant transcription factor NFE2L2 in human mammary epithelial cells.The Journal of biological chemistry · 2012Article
- Progesterone receptors, their isoforms and progesterone regulated transcription.Molecular and cellular endocrinology · 2012Review
- RINGs of good and evil: RING finger ubiquitin ligases at the crossroads of tumour suppression and oncogenesis.Nature reviews. Cancer · 2011Review
- Comparison of increased aromatase versus ERα in the generation of mammary hyperplasia and cancer.Cancer research · 2011Article
- Altered AIB1 or AIB1Δ3 expression impacts ERα effects on mammary gland stromal and epithelial content.Molecular endocrinology (Baltimore, Md.) · 2011Article
- The role of sex steroid receptors on lipogenesis in breast and prostate carcinogenesis: a viewpoint.Hormones & cancer · 2010Review
- Redox regulation in cancer: a double-edged sword with therapeutic potential.Oxidative medicine and cellular longevityReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Previously, we reported that BRCA1 inhibits progesterone receptor (PR) activity and blocks progesterone-stimulated gene expression and cell proliferation. In the present manuscript, we studied the mechanism of BRCA1 inhibition of PR activity, using c-Myc as a model progesterone-regulated promoter. Here, we found that BRCA1 has little or no effect on PR ligand-binding affinity. However, BRCA1 overexpression inhibited the R5020-induced recruitment of PR to the c-Myc and mouse mammary tumor virus progesterone response elements (PREs) and blocked R5020-stimulated c-Myc expression, whereas BRCA1 underexpression did the opposite. In EMSAs, BRCA1 overexpression blocked the R5020-induced complex formation between PR and several radiolabeled PRE-containing oligonucleotides, and in vitro-translated BRCA1 blocked the interaction of full-length PR-A or a fragment containing the DNA-binding domain of PR with a radiolabeled PRE oligonucleotide. In further studies, BRCA1 overexpression inhibited the recruitment of coactivators (steroid receptor coactivator 1 and amplified in breast cancer 1) and enhanced the recruitment of a corepressor (histone deacetylase 1) to the c-Myc PRE, whereas BRCA1 knockdown increased the abundance of AIB1 and decreased the abundance of HDAC1 at the c-Myc PRE. These findings suggest that BRCA1 inhibits progestin-stimulated PR activity, in part, by preventing PR from binding to the PRE and by promoting the formation of a corepressor complex rather than a coactivator complex.
Indexed as
Identifiers
What OpenQuestion holds
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.