ArticleScientific reports2016
Global analysis of transcription in castration-resistant prostate cancer cells uncovers active enhancers and direct androgen receptor targets.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 41 citations in OpenAlex.
- Targeting the Androgen Receptor and Associated Cofactors in Prostate Cancer: Novel Approaches and Future Perspectives.International journal of molecular sciences · 2026Review
- Androgen receptor acts as the transcriptional repressor of the nuclear receptor LRH-1 via the androgen-driven chromatin looping conformation in prostate cancer.Genes & diseases · 2026Article
- Molecular determinants of AR-enhancer interaction and cistrome reprogramming in prostate cancer progression.Endocrine-related cancer · 2026Review
- Androgen receptor-mediated assisted loading of the glucocorticoid receptor modulates transcriptional responses in prostate cancer cells.Genome research · 2025Article
- SNP rs9364554 Modulates Androgen Receptor Binding and Drug Response in Prostate Cancer.Biomolecules · 2025Article
- Untangling the role of tau in sex hormone responsive cancers: lessons learnt from Alzheimer's disease.Clinical science (London, England : 1979) · 2024Review
- Review
- Central role of SUMOylation in the regulation of chromatin interactions and transcriptional outputs of the androgen receptor in prostate cancer cells.Nucleic acids research · 2024Article
- The Androgen Receptor Does Not Directly Regulate the Transcription of DNA Damage Response Genes.Molecular cancer research : MCR · 2023Article
- Long-range gene regulation in hormone-dependent cancer.Nature reviews. Cancer · 2023Review
- MYC reshapes CTCF-mediated chromatin architecture in prostate cancer.Nature communications · 2023Article
- Adaptive and non-adaptive gene expression responses in prostate cancer during androgen deprivation.PloS one · 2023Article
- Extensive androgen receptor enhancer heterogeneity in primary prostate cancers underlies transcriptional diversity and metastatic potential.Nature communications · 2022Article
- From Omics to Multi-Omics Approaches for In-Depth Analysis of the Molecular Mechanisms of Prostate Cancer.International journal of molecular sciences · 2022Review
- Review
- Androgen receptor and MYC equilibration centralizes on developmental super-enhancer.Nature communications · 2021Article
- MiR-205-driven downregulation of cholesterol biosynthesis through SQLE-inhibition identifies therapeutic vulnerability in aggressive prostate cancer.Nature communications · 2021Article
- Genomic Landscapes of Noncoding RNAs RegulatingMolecular and cellular biology · 2021Article
- Androgen Deprivation Induces Transcriptional Reprogramming in Prostate Cancer Cells to Develop Stem Cell-Like Characteristics.International journal of molecular sciences · 2020Article
- Antibody profiling of patients with prostate cancer reveals differences in antibody signatures among disease stages.Journal for immunotherapy of cancer · 2020Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Androgen receptor (AR) is a male sex steroid-activated transcription factor (TF) that plays a critical role in prostate cancers, including castration-resistant prostate cancers (CRPC) that typically express amplified levels of the AR. CRPC-derived VCaP cells display an excessive number of chromatin AR-binding sites (ARBs) most of which localize to distal inter- or intragenic regions. Here, we analyzed direct transcription programs of the AR in VCaP cells using global nuclear run-on sequencing (GRO-seq) and integrated the GRO-seq data with the ARB and VCaP cell-specific TF-binding data. Androgen immediately activated transcription of hundreds of protein-coding genes, including IGF-1 receptor and EGF receptor. Androgen also simultaneously repressed transcription of a large number of genes, including MYC. As functional enhancers have been postulated to produce enhancer-templated non-coding RNAs (eRNAs), we also analyzed the eRNAs, which revealed that only a fraction of the ARBs reside at functional enhancers. Activation of these enhancers was most pronounced at the sites that also bound PIAS1, ERG and HDAC3, whereas binding of HDAC3 and PIAS1 decreased at androgen-repressed enhancers. In summary, our genome-wide data of androgen-regulated enhancers and primary target genes provide new insights how the AR can directly regulate cellular growth and control signaling pathways in CPRC cells.
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