ArticleBritish journal of cancer2014
Prostate cancer bone metastases acquire resistance to androgen deprivation via WNT5A-mediated BMP-6 induction.
Article in British journal of cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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43 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.
- Estrogen related receptor alpha in castration-resistant prostate cancer cells promotes tumor progression in bone.Oncotarget · 2016Pooled it
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- From lab to life: technological innovations in transforming cancer metastasis detection and therapy.Discover oncology · 2025Review
- Recent advances in understanding the role of Wnt5a in prostate cancer and bone metastasis.Discover oncology · 2025Review
- BMP Stimulation Differentially Affects Phosphorylation and Protein Stability of β-Catenin in Breast Cancer Cell Lines.International journal of molecular sciences · 2024Article
- BMP signaling in cancer stemness and differentiation.Cell regeneration (London, England) · 2023Review
- Wnt Signaling and Therapeutic Resistance in Castration-Resistant Prostate Cancer.Current pharmacology reports · 2023Article
- WNT ligands in non-small cell lung cancer: from pathogenesis to clinical practice.Discover oncology · 2023Review
- Review
- Epigenetic Silencing of BMP6 by the SIN3A-HDAC1/2 Repressor Complex Drives Melanoma Metastasis via FAM83G/PAWS1.Molecular cancer research : MCR · 2022Article
- Altered Wnt5a expression affects radiosensitivity of non-small cell lung cancer via the Wnt/β-catenin pathway.Experimental and therapeutic medicine · 2022Article
- SOX4: The unappreciated oncogene.Seminars in cancer biology · 2020Review
- Mechanisms of the Osteogenic Switch of Smooth Muscle Cells in Vascular Calcification: WNT Signaling, BMPs, Mechanotransduction, and EndMT.Bioengineering (Basel, Switzerland) · 2020Review
- MCM3AP-AS1/miR-876-5p/WNT5A axis regulates the proliferation of prostate cancer cells.Cancer cell international · 2020Article
- Expression Level of Wnt5a Was Related to the Therapeutic Effects of First-Generation EGFR-TKIs.OncoTargets and therapy · 2020Article
- Mating induces switch from hormone-dependent to hormone-independent steroid receptor-mediated growth in Drosophila secondary cells.PLoS biology · 2019Article
- An Autocrine Wnt5a Loop Promotes NF-κB Pathway Activation and Cytokine/Chemokine Secretion in Melanoma.Cells · 2019Article
- Systematically understanding the immunity leading to CRPC progression.PLoS computational biology · 2019Article
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Authors and funding
12 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAndrogen ablation is the first-line therapy for patients with metastatic prostate cancer (CaP). However, castration resistance will eventually emerge. In the present study, we have investigated the role of bone morphogenetic protein-6 (BMP-6) in the development of castration-resistant prostate cancer (CRPC) in the context of bone metastases.
methodsWe initially investigated the clinical course of 158 men with advanced CaP who were treated with primary androgen deprivation therapy. To elucidate the underlying mechanism of CRPC in the context of bone metastases, we examined the impact of bone stromal cells on CaP in the absence of androgens using a co-culture model.
resultsIn the 158 patients, we found that the median time to prostate-specific antigen progression was significantly shorter when bone metastases were present (14 months (95% CI, 10.2-17.8 months) vs 57 months (95% CI, 19.4-94.6 months)). These results suggest that bone-tumour interactions may accelerate castration resistance. Consistent with this hypothesis, in vitro co-cultures demonstrated that CaP cells proliferated under an androgen-depleted condition when incubated with bone stromal cells. Mechanistically, gene expression analysis using quantitative polymerase chain reaction arrays showed a dramatic induction of BMP-6 by CaP cell lines in the presence of bone stromal cells. Further studies revealed that WNT5A derived from bone stromal cells induced the expression of BMP-6 by CaP cells; BMP-6 in turn stimulated cellular proliferation of CaP cells in an androgen-deprived media via a physical interaction between Smad5 and β-catenin. Intracellularly, WNT5A increased BMP-6 expression via protein kinase C/NF-κB pathway in CaP cell lines.
conclusionsThese observations suggest that bone-CaP interaction leads to castration resistance via WNT5A/BMP-6 loop.
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