ArticleMolecular and cellular endocrinology2013
Transcriptional activity of c-Jun is critical for the suppression of AR function.
Article in Molecular and cellular endocrinology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Androgen receptor dynamics in prostate cancer: from disease progression to treatment resistance.Frontiers in oncology · 2025Review
- Prostate cancers with distinct transcriptional programs in Black and White men.Genome medicine · 2024Article
- Discovery and Biological Characterization of PRMT5:MEP50 Protein-Protein Interaction Inhibitors.Journal of medicinal chemistry · 2022Article
- Article
- Prostate Cancer Epigenetic Plasticity and Enhancer Heterogeneity: Molecular Causes, Consequences and Clinical Implications.Advances in experimental medicine and biology · 2022Review
- Cellular specificity of androgen receptor, coregulators, and pioneer factors in prostate cancer.Endocrine oncology (Bristol, England) · 2022Review
- Reprogramming landscape highlighted by dynamic transcriptomes in therapy-induced neuroendocrine differentiation.Computational and structural biotechnology journal · 2022Article
- A bioinformatics approach for identifying potential molecular mechanisms and key genes involved in COVID-19 associated cardiac remodeling.Gene reports · 2021Article
- The role of N-cadherin/c-Jun/NDRG1 axis in the progression of prostate cancer.International journal of biological sciences · 2021Article
- The Impact of Whole Genome Data on Therapeutic Decision-Making in Metastatic Prostate Cancer: A Retrospective Analysis.Cancers · 2020Article
- Factors that influence the androgen receptor cistrome in benign and malignant prostate cells.Molecular oncology · 2019Article
- Essential role of JunD in cell proliferation is mediated via MYC signaling in prostate cancer cells.Cancer letters · 2019Article
- Article
- Cholesterol Sulfonation Enzyme, SULT2B1b, Modulates AR and Cell Growth Properties in Prostate Cancer.Molecular cancer research : MCR · 2016Article
- A Signaling Network Controlling Androgenic Repression of c-Fos Protein in Prostate Adenocarcinoma Cells.The Journal of biological chemistry · 2016Article
- Lysine-specific demethylase 1 mediates epidermal growth factor signaling to promote cell migration in ovarian cancer cells.Scientific reports · 2015Article
- Transcriptional activation of PRMT5 by NF-Y is required for cell growth and negatively regulated by the PKC/c-Fos signaling in prostate cancer cells.Biochimica et biophysica acta · 2014Article
- Targeting CREB inhibits radiation-induced neuroendocrine differentiation and increases radiation-induced cell death in prostate cancer cells.American journal of cancer research · 2014Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Androgen receptor (AR) signaling plays a pivotal role in growth and survival of prostate cancer cells. c-Jun is an important member of the activator protein 1 (AP-1) family and was shown to interact with AR. However, the role of c-Jun in AR signaling remains controversial, with being a coactivator or a corepressor reported. Here, utilizing multiple approaches, we show that c-Jun efficiently inhibits AR activity and the growth of prostate cancer cells. Overexpression of c-Jun inhibits not only the activities of various androgen-responsive promoters but also the transcripts of multiple AR target genes. Interestingly, long-term c-Jun overexpression also down-regulates AR expression at both the protein and mRNA levels. Molecular analysis suggests that c-Jun inhibits AR transactivation potential via an unknown target gene. The inhibition of AR by c-Jun occurs in both hormone naïve and castration-resistant prostate cancer cells. Our results unravel a novel mechanism by which c-Jun antagonizes the AR signaling.
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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.