ArticlePloS one2012
The chicken ovalbumin upstream promoter-transcription factor II negatively regulates the transactivation of androgen receptor in prostate cancer cells.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 25 citations in OpenAlex.
- International Union of Basic and Clinical Pharmacology CXIII: Nuclear Receptor Superfamily-Update 2023.Pharmacological reviews · 2023Review
- N/C Interactions Are Dispensable for Normal In Vivo Functioning of the Androgen Receptor in Male Mice.Endocrinology · 2022Article
- Small-molecule inhibitor targeting orphan nuclear receptor COUP-TFII for prostate cancer treatment.Science advances · 2020Article
- Recent progress on the role and molecular mechanism of chicken ovalbumin upstream promoter-transcription factor II in cancer.The Journal of international medical research · 2020Review
- The nuclear receptor seven up functions in adipocytes and oenocytes to control distinct steps of Drosophila oogenesis.Developmental biology · 2019Article
- Review
- Article
- COUP-TFII regulates metastasis of colorectal adenocarcinoma cells by modulating Snail1.British journal of cancer · 2014Article
- Minireview: role of orphan nuclear receptors in cancer and potential as drug targets.Molecular endocrinology (Baltimore, Md.) · 2014Review
- COUP-TFII inhibits NFkappaB activation in endocrine-resistant breast cancer cells.Molecular and cellular endocrinology · 2014Article
- The critical roles of COUP-TFII in tumor progression and metastasis.Cell & bioscience · 2014Review
- Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Androgen receptor (AR) is involved in the development and progression of prostate cancers. However, the mechanisms by which this occurs remain incompletely understood. In previous reports, chicken ovalbumin upstream promoter-transcription factor II (COUP-TF II) has been suggested to play a role in the development of cancers. In the present study, we explored a putative role of COUP-TF II in prostate cancers by investigating its effect on cell proliferation and a cross-talk between COUP-TF II and AR. Overexpression of COUP-TF II results in the inhibition of androgen-dependent proliferation of prostate cancer cells. Further studies show that COUP-TF II functions as a corepressor of AR. It represses AR transactivation on target promoters containing the androgen response element (ARE) in a dose-dependent manner. In addition, COUP-TF II interacts physically with AR in vitro and in vivo. It binds to both the DNA binding domain (DBD) and the ligand-binding domain (LBD) of AR and disrupts the N/C terminal interaction of AR. Furthermore, COUP-TF II competes with coactivators such as ARA70, SRC-1, and GRIP1 to modulate AR transactivation as well as inhibiting the recruitment of AR to its ARE-containing target promoter. Taken together, our findings suggest that COUP-TF II is a novel corepressor of AR, and provide an insight into the role of COUP-TF II in prostate cancers.
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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.