ArticleOncotarget2015
FOXA1 regulates androgen receptor variant activity in models of castrate-resistant prostate cancer.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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The trial behind it
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Who cites it
30 citing papers in PubMed, 46 citations in OpenAlex.
- Epigenetic profiling identifies markers of endocrine resistance and therapeutic options for metastatic castration-resistant prostate cancer.Cell reports. Medicine · 2025Trial
- Molecular determinants of AR-enhancer interaction and cistrome reprogramming in prostate cancer progression.Endocrine-related cancer · 2026Review
- 3D genome architecture and epigenetic regulation of lineage identity in advanced prostate cancer.Endocrinology · 2026Review
- Alterations in AR-FOXA1 signaling in prostate cancer progression and therapeutic resistance.Journal of the National Cancer Center · 2026Review
- Targeting PCNA/AR interaction inhibits AR-mediated signaling in castration resistant prostate cancer cells.Oncotarget · 2025Article
- Defining Splicing Factor Requirements for Androgen Receptor Variant Synthesis in Advanced Prostate Cancer.Molecular cancer research : MCR · 2024Article
- Androgen Receptor Splice Variants Contribute to the Upregulation of DNA Repair in Prostate Cancer.Cancers · 2022Article
- Development of a High-Throughput Screening Assay for Small-Molecule Inhibitors of Androgen Receptor Splice Variants.Assay and drug development technologies · 2022Article
- Cistrome and transcriptome analysis identifies unique androgen receptor (AR) and AR-V7 splice variant chromatin binding and transcriptional activities.Scientific reports · 2022Article
- Epigenetic Coregulation of Androgen Receptor Signaling.Advances in experimental medicine and biology · 2022Article
- Cellular specificity of androgen receptor, coregulators, and pioneer factors in prostate cancer.Endocrine oncology (Bristol, England) · 2022Review
- Nuclear Export Inhibitor KPT-8602 Synergizes with PARP Inhibitors in Escalating Apoptosis in Castration Resistant Cancer Cells.International journal of molecular sciences · 2021Article
- BRG1 knockdown inhibits proliferation through multiple cellular pathways in prostate cancer.Clinical epigenetics · 2021Article
- Combination therapy with androgen receptor N-terminal domain antagonist EPI-7170 and enzalutamide yields synergistic activity in AR-V7-positive prostate cancer.Molecular oncology · 2020Article
- AKR1C3 Promotes AR-V7 Protein Stabilization and Confers Resistance to AR-Targeted Therapies in Advanced Prostate Cancer.Molecular cancer therapeutics · 2019Article
- Cellular and Molecular Mechanisms Underlying Prostate Cancer Development: Therapeutic Implications.Medicines (Basel, Switzerland) · 2019Review
- A novel CRISPR-engineered prostate cancer cell line defines the AR-V transcriptome and identifies PARP inhibitor sensitivities.Nucleic acids research · 2019Article
- Comprehensive Genomic Analysis Reveals that the Pioneering Function of FOXA1 Is Independent of Hormonal Signaling.Cell reports · 2019Article
- The Dominant Role of Forkhead Box Proteins in Cancer.International journal of molecular sciences · 2018Review
- Down-regulation of AR splice variants through XPO1 suppression contributes to the inhibition of prostate cancer progression.Oncotarget · 2018Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Retention of androgen receptor (AR) signalling in castrate-resistant prostate cancer (CRPC) highlights the requirement for the development of more effective AR targeting therapies. A key mechanism of resistance to anti-androgens is through expression of constitutively active AR variants (AR-Vs) that are refractory to next-generation therapies, including Enzalutamide and Abiraterone. By maintaining an androgenic gene signature, AR-Vs drive tumour survival and progression in castrate conditions. Critically, however, our understanding of the mechanics of AR-V-driven transcription is limited, particularly with respect to dependency on pioneer factor function. Here we show that depletion of FOXA1 in the CWR22Rv1 CRPC cell line abrogates the oncogenic potential of AR-Vs. Gene expression profiling reveals that approximately 41% of the AR-V transcriptome requires FOXA1 and that depletion of FOXA1 attenuates AR-V binding at a sub-set of analysed co-regulated genes. Interestingly, AR-V levels are elevated in cells depleted of FOXA1 as a consequence of attenuated negative feedback on the AR gene, but is insufficient to maintain cell growth as evidenced by marked anti-proliferative effects in FOXA1 knockdown cells. In all, our data suggests that AR-Vs are dependent on FOXA1 for sustaining a pro-proliferative gene signature and agents targeting FOXA1 may represent novel therapeutic options for CRPC patients.
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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.