ArticleScientific reports2015
The RNA-binding protein Sam68 regulates expression and transcription function of the androgen receptor splice variant AR-V7.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 58 citations in OpenAlex.
- Targeting the Androgen Receptor and Associated Cofactors in Prostate Cancer: Novel Approaches and Future Perspectives.International journal of molecular sciences · 2026Review
- Roles of KHDRBS2 and KHDRBS3 in prostate cancer progression and AR-V7 regulation.Discover oncology · 2025Article
- YTHDC1 orchestrates oncogenic splicing via the CLK1-SRSF1 splicing machinery to regulate castration-resistant prostate cancer progression.Molecular and cellular biochemistry · 2025Article
- Insulin-Like Growth Factor 2 mRNA-Binding Protein 2 (IGF2BP2) Promotes Castration-Resistant Prostate Cancer Progression by Regulating AR-V7 mRNA Stability.Cancer reports (Hoboken, N.J.) · 2025Article
- Inhibition of Galectin-1 and Androgen Receptor Axis Enhances Enzalutamide Treatment in Enzalutamide Resistant Prostate Cancer.Cancers · 2025Article
- Defining Splicing Factor Requirements for Androgen Receptor Variant Synthesis in Advanced Prostate Cancer.Molecular cancer research : MCR · 2024Article
- Role of Sam68 as an adaptor protein in inflammatory signaling.Cellular and molecular life sciences : CMLS · 2024Review
- KHDRBS1 as a novel prognostic signaling biomarker influencing hepatocellular carcinoma cell proliferation, migration, immune microenvironment, and drug sensitivity.Frontiers in immunology · 2024Article
- The transcriptional terminator XRN2 and the RNA-binding protein Sam68 link alternative polyadenylation to cell cycle progression in prostate cancer.Nature structural & molecular biology · 2022Article
- The Crucial Role of AR-V7 in Enzalutamide-Resistance of Castration-Resistant Prostate Cancer.Cancers · 2022Review
- DNA Damage Regulates the Functions of the RNA Binding Protein Sam68 through ATM-Dependent Phosphorylation.Cancers · 2022Article
- Second generation androgen receptor antagonists and challenges in prostate cancer treatment.Cell death & disease · 2022Review
- DNA- and RNA-Binding Proteins Linked Transcriptional Control and Alternative Splicing Together in a Two-Layer Regulatory Network System of Chronic Myeloid Leukemia.Frontiers in molecular biosciences · 2022Article
- The androgen receptor messenger RNA: what do we know?RNA biology · 2022Review
- Nuclear Export Inhibitor KPT-8602 Synergizes with PARP Inhibitors in Escalating Apoptosis in Castration Resistant Cancer Cells.International journal of molecular sciences · 2021Article
- Review
- Increased transcription and high translation efficiency lead to accumulation of androgen receptor splice variant after androgen deprivation therapy.Cancer letters · 2021Article
- Regulation of RNA Splicing: Aberrant Splicing Regulation and Therapeutic Targets in Cancer.Cells · 2021Review
- 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
- Regulation of androgen receptor variants in prostate cancer.Asian journal of urology · 2020Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Castration-resistant (CR) prostate cancer (PCa) partly arises due to persistence of androgen receptor (AR) transcriptional activity in the absence of cognate ligand. An emerging mechanism underlying the CRPCa phenotype and predicting response to therapy is the expression of the constitutively-active AR-V7 splice variant generated by AR cryptic exon 3b inclusion. Here, we explore the role of the RNA-binding protein (RBP) Sam68 (encoded by KHDRBS1), which is over-expressed in clinical PCa, on AR-V7 expression and transcription function. Using a minigene reporter, we show that Sam68 controls expression of exon 3b resulting in an increase in endogenous AR-V7 mRNA and protein expression in RNA-binding-dependent manner. We identify a novel protein-protein interaction between Sam68 and AR-V7 mediated by a common domain shared with full-length AR, and observe these proteins in the cell nucleoplasm. Using a luciferase reporter, we demonstrate that Sam68 co-activates ligand-independent AR-V7 transcriptional activity in an RNA-binding-independent manner, and controls expression of the endogenous AR-V7-specific gene target UBE2C. Our data suggest that Sam68 has separable effects on the regulation of AR-V7 expression and transcriptional activity, through its RNA-binding capacity. Sam68 and other RBPs may control expression of AR-V7 and other splice variants as well as their downstream functions in CRPCa.
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