ArticleCancer reports (Hoboken, N.J.)2025
Insulin-Like Growth Factor 2 mRNA-Binding Protein 2 (IGF2BP2) Promotes Castration-Resistant Prostate Cancer Progression by Regulating AR-V7 mRNA Stability.
Article in Cancer reports (Hoboken, N.J.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Rewiring the tumor microenvironment: IGFBP2 at the Nexus of remodeling and therapy resistance?Biochimica et biophysica acta. Reviews on cancer · 2026Review
- Inhibition of the RORC/GPX4 mediated ferroptosis regulatory axis suppresses tumor growth and alleviates enzalutamide resistance in prostate cancer.Cellular & molecular biology letters · 2026Article
- YTHDC1 orchestrates oncogenic splicing via the CLK1-SRSF1 splicing machinery to regulate castration-resistant prostate cancer progression.Molecular and cellular biochemistry · 2025Article
- Integrative analysis identifies FBXO5 as a critical mediator of CRPC progression and bone metastatic potential.Discover oncology · 2025Article
- Clinical data investigation identifies MARK3 as an oncogenic driver in castration-resistant prostate cancer.Biochemistry and biophysics reports · 2025Article
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5 authors.
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Abstract
backgroundThe emergence of constitutively active androgen receptor (AR) splice variant AR-V7 poses a formidable challenge in treating prostate cancer, as it lacks the ligand binding region targeted by androgen-deprivation therapies such as enzalutamide and abiraterone. AR-V7 is critical for castration-resistant prostate cancer (CRPC) development and progression; however, the molecular mechanisms regulating its expression and biological function remain poorly understood. Here, we investigate the role of IGF2BP2 in regulating AR-V7 expression and CRPC progression.
methodsTo determine the clinical relevance of IGF2BP2 in CRPC, we analyzed the mRNA expression data for prostate cancer patients available in the Genomic Data Commons (GDC) Data Portal and cBioPortal. Next to investigate the role of IGF2BP2 in regulating AR-V7 expression and enzalutamide resistance, we performed shRNA-mediated IGF2BP2 knockdown and overexpression experiments followed by qRT-PCR, immunoblot, colony-formation, and MTT assays. Finally, we performed RIP-qPCR, actinomycin-D, and IGF2BP2 domain-deletion analysis to study the mechanism by which IGF2BP2 regulates AR-V7 stability, expression, and enzalutamide resistance in CRPC cells.
resultsOur analysis revealed that IGF2BP2 is upregulated in CRPC patients and its expression positively correlates with increasing Gleason score in patients with CRPC. We demonstrate that IGF2BP2 silencing leads to downregulation of AR-V7 and its downstream target genes without affecting AR levels. Additionally, IGF2BP2 knockdown also enhances the sensitivity of CRPC cells to enzalutamide while overexpression increases AR-V7 expression and confers increased resistance to enzalutamide. Mechanistically, our experiments demonstrate that IGF2BP2 binds to the intronic splicing enhancer (ISE) region of AR-V7, thereby enhancing its mRNA stability. Furthermore, our domain-deletion analysis pinpoints the role of KH3 and KH4 domains of IGF2BP2 in regulating AR-V7 stability and enzalutamide resistance.
conclusionsTaken together, our findings suggest that IGF2BP2 plays a critical role in regulating AR-V7 expression and stability, offering a novel target for developing therapeutic interventions for CRPC.
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