ArticleMolecular cancer research : MCR2017
Targeting AR Variant-Coactivator Interactions to Exploit Prostate Cancer Vulnerabilities.
Article in Molecular cancer research : MCR, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Developing a Fluorescence-Based High-Throughput Screening Method for Natural Product Fractions to Identify Inhibitors of AR-V7 for Castration-Resistant Prostate Cancer.Pharmaceutics · 2026Article
- Rho Small GTPase Family in Androgen-Regulated Prostate Cancer Progression and Metastasis.Cancers · 2025Review
- VAV2 Drives EGFR-Mediated Rac1 Responses in Prostate Cancer.Molecular cancer research : MCR · 2025Article
- RAC1 signaling in prostate cancer: VAV GEFs take center stage.Frontiers in cell and developmental biology · 2025Article
- Androgen Receptor-Interacting Proteins in Prostate Cancer Development and Therapy Resistance.The American journal of pathology · 2024Review
- International Union of Basic and Clinical Pharmacology CXIII: Nuclear Receptor Superfamily-Update 2023.Pharmacological reviews · 2023Review
- Acetyl-CoA Counteracts the Inhibitory Effect of Antiandrogens on Androgen Receptor Signaling in Prostate Cancer Cells.Cancers · 2022Article
- The Crucial Role of AR-V7 in Enzalutamide-Resistance of Castration-Resistant Prostate Cancer.Cancers · 2022Review
- The kinesin KIF20A promotes progression to castration-resistant prostate cancer through autocrine activation of the androgen receptor.Oncogene · 2022Article
- Genetic Factors Associated with Prostate Cancer Conversion from Active Surveillance to Treatment.HGG advances · 2022Article
- Simulated Microgravity Influences VEGF, MAPK, and PAM Signaling in Prostate Cancer Cells.International journal of molecular sciences · 2020Article
- Therapies Targeted to Androgen Receptor Signaling Axis in Prostate Cancer: Progress, Challenges, and Hope.Cancers · 2019Review
- Current strategies for targeting the activity of androgen receptor variants.Asian journal of urology · 2019Review
- Construction of a set of novel and robust gene expression signatures predicting prostate cancer recurrence.Molecular oncology · 2018Article
- Role of Androgen Receptor Variants in Prostate Cancer: Report from the 2017 Mission Androgen Receptor Variants Meeting.European urology · 2018Review
- PRADclass: Hybrid Gleason Grade-Informed Computational Strategy Identifies Consensus Biomarker Features Predictive of Aggressive Prostate Adenocarcinoma.Technology in cancer research & treatmentArticle
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Castration-resistant prostate cancer (CRPC) progresses rapidly and is incurable. Constitutively active androgen receptor splice variants (AR-Vs) represent a well-established mechanism of therapeutic resistance and disease progression. These variants lack the AR ligand-binding domain and, as such, are not inhibited by androgen deprivation therapy (ADT), which is the standard systemic approach for advanced prostate cancer. Signaling by AR-Vs, including the clinically relevant AR-V7, is augmented by Vav3, an established AR coactivator in CRPC. Using mutational and biochemical studies, we demonstrated that the Vav3 Diffuse B-cell lymphoma homology (DH) domain interacted with the N-terminal region of AR-V7 (and full length AR). Expression of the Vav3 DH domain disrupted Vav3 interaction with and enhancement of AR-V7 activity. The Vav3 DH domain also disrupted AR-V7 interaction with other AR coactivators: Src1 and Vav2, which are overexpressed in PC. This Vav3 domain was used in proof-of-concept studies to evaluate the effects of disrupting the interaction between AR-V7 and its coactivators on CRPC cells. This disruption decreased CRPC cell proliferation and anchorage-independent growth, caused increased apoptosis, decreased migration, and resulted in the acquisition of morphological changes associated with a less aggressive phenotype. While disrupting the interaction between FL-AR and its coactivators decreased N-C terminal interaction, disrupting the interaction of AR-V7 with its coactivators decreased AR-V7 nuclear levels.
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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.