ArticleSignal transduction and targeted therapy2025
Targeting TRPV6/CXCR4 complexes prevents castration-resistant prostate cancer metastasis to the bone.
Article in Signal transduction and targeted therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Targeting a Myeloid-Regulatory B Cell Network Reverses Immune Paralysis in Periprosthetic Joint Infections.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- Breaking the immune "cold niche" in bone metastasis: core mechanisms of the multidimensional interwoven regulatory network and precision breakthrough strategies.Molecular cancer · 2026Review
- From Bone Marrow Reserve to Metastatic Niche: How Neutrophil-Lineage Cells Shape Skeletal Colonization.International journal of molecular sciences · 2026Review
- Article
- Targeting ion channel dysregulation in tumors: emerging therapeutic opportunities.Trends in pharmacological sciences · 2026Review
- The interrelationship between prostate cancer and osteoporosis: new perspectives on shared molecular pathways and treatment strategies.International journal of surgery (London, England) · 2026Article
- Discovery of the small molecular inhibitors against TRPV6 as potential anti-cancer agents by structural based virtual screening.Frontiers in chemistry · 2026Article
- The CXCR4-targeted theranostics era: a comprehensive review of a decade of progress (2015-2025).Theranostics · 2026Review
- Research advances in the role of osteoblasts and their derivatives in the development, recurrence, and distant metastasis of malignant bone tumors: a narrative review.EFORT open reviews · 2025Review
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Authors and funding
14 authors.
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Abstract
Bone metastasis most commonly occurs in castration-resistant prostate cancer (CRPC). The TRPV6 calcium channel is absent in healthy prostate tissue, but its expression increases considerably during cancer progression. We hypothesized that cancer cells induce TRPV6 expression de novo to directly benefit from tightly regulated calcium intake via TRPV6 while providing cancer cells with a selective advantage for metastasis in the calcium-abundant niche, such as bone. Using a cohort of prostate cancer tissue biopsies from patients with a clinical history of at least 10 years after biopsy, we report that TRPV6 expression directly correlates with CRPC tumor aggressiveness and increased risk of metastasis development. The TRPV6 channel is involved in the acquisition of both mesenchymal and invasive phenotypes through increased phosphorylation of CaMK2 followed by the translocation of the transcription factor NF-κB to the nucleus and the expression of EMT markers, MMPs, and transcription factors such as Twist, Snail, and Slug. Moreover, TRPV6 expression was accompanied by increased formation of CXCR4/TRPV6 complexes. In vivo, mice bearing trpv6
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