ArticleMolecular endocrinology (Baltimore, Md.)2012
Vav3 enhances androgen receptor splice variant activity and is critical for castration-resistant prostate cancer growth and survival.
Article in Molecular endocrinology (Baltimore, Md.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 53 citations in OpenAlex.
- Rho Small GTPase Family in Androgen-Regulated Prostate Cancer Progression and Metastasis.Cancers · 2025Review
- RAC1 signaling in prostate cancer: VAV GEFs take center stage.Frontiers in cell and developmental biology · 2025Article
- International Union of Basic and Clinical Pharmacology CXIII: Nuclear Receptor Superfamily-Update 2023.Pharmacological reviews · 2023Review
- Characterization of allosteric modulators that disrupt androgen receptor co-activator protein-protein interactions to alter transactivation-Drug leads for metastatic castration resistant prostate cancer.SLAS discovery : advancing life sciences R & D · 2023Article
- Analysis of novel enzalutamide-resistant cells: upregulation of testis-specific Y-encoded protein gene promotes the expression of androgen receptor splicing variant 7.Translational cancer research · 2020Article
- Therapies Targeted to Androgen Receptor Signaling Axis in Prostate Cancer: Progress, Challenges, and Hope.Cancers · 2019Review
- Arginine vasopressin receptor 1a is a therapeutic target for castration-resistant prostate cancer.Science translational medicine · 2019Article
- Current strategies for targeting the activity of androgen receptor variants.Asian journal of urology · 2019Review
- TGF-β receptor I inhibitor enhances response to enzalutamide in a pre-clinical model of advanced prostate cancer.The Prostate · 2019Article
- Down-regulation of AR splice variants through XPO1 suppression contributes to the inhibition of prostate cancer progression.Oncotarget · 2018Article
- Identification of an oncogenic network with prognostic and therapeutic value in prostate cancer.Molecular systems biology · 2018Article
- Targeting AR Variant-Coactivator Interactions to Exploit Prostate Cancer Vulnerabilities.Molecular cancer research : MCR · 2017Article
- Thioredoxin-1 protects against androgen receptor-induced redox vulnerability in castration-resistant prostate cancer.Nature communications · 2017Article
- Androgen Receptor Variants Mediate DNA Repair after Prostate Cancer Irradiation.Cancer research · 2017Article
- Aberrant TGF-β Signaling Drives Castration-Resistant Prostate Cancer in a Male Mouse Model of Prostate Tumorigenesis.Endocrinology · 2017Article
- Review
- Emerging data on androgen receptor splice variants in prostate cancer.Endocrine-related cancer · 2016Review
- Reconfiguring the AR-TIF2 Protein-Protein Interaction HCS Assay in Prostate Cancer Cells and Characterizing the Hits from a LOPAC Screen.Assay and drug development technologies · 2016Article
- The microRNA-23b/-27b cluster suppresses prostate cancer metastasis via Huntingtin-interacting protein 1-related.Oncogene · 2016Article
- Targeting constitutively active androgen receptor splice variants in castration resistant prostate cancer.Expert opinion on therapeutic targets · 2016Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Advanced or metastatic prostate cancer is treated by androgen deprivation; however, patients inevitably relapse with castration-resistant prostate cancer (CRPC). CRPC remains dependent on androgen receptor (AR) signaling, which may include constitutive, ligand-independent action of naturally occurring AR splice variants. For example, the AR splice variant AR3 (also termed AR-V7) is expressed in CRPC and is linked to poor prognosis. Vav3, a Rho GTPase guanine nucleotide exchange factor, is an AR coactivator that is up-regulated in human prostate cancer compared with benign tissue and in preclinical models of CRPC. Vav3 confers castration-resistant growth to androgen-dependent human prostate cancer cells. Despite the importance of AR coactivators in promoting CRPC, the potential role of these regulatory proteins in modulating AR splice variant activity is unknown. We examined the contributions of Vav3 to AR activity in two CRPC cell lines that naturally express relatively high levels of Vav3 and AR3. Vav3 or AR3 knockdown greatly attenuated cell proliferation, soft agar growth, and ligand-independent AR activity. Vav3 potently enhanced the transcriptional activity of AR3 and another clinically relevant AR splice variant, ARv567es. Vav3 knockdown resulted in lowered nuclear AR3 levels, whereas total AR3 levels remained similar. Conversely, overexpression of Vav3 resulted in increased nuclear AR3. Coimmunoprecipitation revealed that AR3 and Vav3 interact. These novel data demonstrating physical and functional interactions between Vav3, a unique AR coactivator, and an AR splice variant provide insights into the mechanisms by which Vav3 exploits and enhances AR signaling in the progression to CRPC.
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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.