ArticleNucleic acids research2012
Persistent androgen receptor-mediated transcription in castration-resistant prostate cancer under androgen-deprived conditions.
Article in Nucleic acids research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
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Who cites it
77 citing papers in PubMed, 108 citations in OpenAlex.
- Castration-resistant prostate cancer as an adaptive tumor ecosystem: coupling tumor evolution with microenvironmental reprogramming.Cancer metastasis reviews · 2026Review
- SLPI in Prostate Cancer.Cancers · 2026Review
- Circular RNA-based therapy targeting metabolic vulnerability of fatty acid synthesis overcomes castration-resistant prostate cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- ECD, a novel androgen receptor target promotes prostate cancer tumorigenesis by regulating glycolysis.Oncogene · 2025Article
- NASP implication in the androgen receptor associated with castration resistance in prostate cancer.Cell communication and signaling : CCS · 2025Article
- Matrix stiffness modulates androgen response genes and chromatin state in prostate cancer.NAR cancer · 2025Article
- DPYSL5 is highly expressed in treatment-induced neuroendocrine prostate cancer and promotes lineage plasticity via EZH2/PRC2.Communications biology · 2024Article
- To eat or not to eat: a critical review on the role of autophagy in prostate carcinogenesis and prostate cancer therapeutics.Frontiers in pharmacology · 2024Review
- Transposable Elements Are Co-opted as Oncogenic Regulatory Elements by Lineage-Specific Transcription Factors in Prostate Cancer.Cancer discovery · 2023Article
- TRAF4-mediated nonproteolytic ubiquitination of androgen receptor promotes castration-resistant prostate cancer.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Up-regulation of secretory leukocyte protease inhibitor in human samples might have a potential role of predicting prostate cancer recurrence and progression after surgery and hormonal therapy.Cancer medicine · 2023Article
- CRISPR screens reveal genetic determinants of PARP inhibitor sensitivity and resistance in prostate cancer.Nature communications · 2023Article
- Adaptive and non-adaptive gene expression responses in prostate cancer during androgen deprivation.PloS one · 2023Article
- TRIM33 drives prostate tumor growth by stabilizing androgen receptor from Skp2-mediated degradation.EMBO reports · 2022Article
- Understanding and targeting prostate cancer cell heterogeneity and plasticity.Seminars in cancer biology · 2022Review
- Cistrome and transcriptome analysis identifies unique androgen receptor (AR) and AR-V7 splice variant chromatin binding and transcriptional activities.Scientific reports · 2022Article
- Article
- Novel Oncogenic Transcription Factor Cooperation in RB-Deficient Cancer.Cancer research · 2022Article
- The androgen receptor inhibits transcription of GPER1 by preventing Sp1 and Sp3 from binding to the promoters in prostate cancer cells.Oncotarget · 2022Article
- The ADAM9/UBN2/AKR1C3 axis promotes resistance to androgen-deprivation in prostate cancer.American journal of cancer research · 2022Article
17 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The androgen receptor (AR) is a ligand-inducible transcription factor that mediates androgen action in target tissues. Upon ligand binding, the AR binds to thousands of genomic loci and activates a cell-type specific gene program. Prostate cancer growth and progression depend on androgen-induced AR signaling. Treatment of advanced prostate cancer through medical or surgical castration leads to initial response and durable remission, but resistance inevitably develops. In castration-resistant prostate cancer (CRPC), AR activity remains critical for tumor growth despite androgen deprivation. Although previous studies have focused on ligand-dependent AR signaling, in this study we explore AR function under the androgen-deprived conditions characteristic of CRPC. Our data demonstrate that AR persistently occupies a distinct set of genomic loci after androgen deprivation in CRPC. These androgen-independent AR occupied regions have constitutively open chromatin structures that lack the canonical androgen response element and are independent of FoxA1, a transcription factor involved in ligand-dependent AR targeting. Many AR binding events occur at proximal promoters, which can act as enhancers to augment transcriptional activities of other promoters through DNA looping. We further show that androgen-independent AR binding directs a gene expression program in CRPC, which is necessary for the growth of CRPC after androgen withdrawal.
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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.