ArticleMaterials today. Bio2025
ECM-mimicking hydrogel models of human adipose tissue identify deregulated lipid metabolism in the prostate cancer-adipocyte crosstalk under antiandrogen therapy.
Article in Materials today. Bio, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Remodeling the marrow fat niche: BMAT in cancer bone metastases and hematological malignancies.Current opinion in endocrine and metabolic research · 2026Article
- SARIFA and Lipid Metabolic Reprogramming in Prostate Cancer: Fundamental Mechanisms, Tumor Microenvironment, and Novel Biomarker Prospects.Life (Basel, Switzerland) · 2026Review
- Si Ni Powder enhances chemotherapy efficacy in sleep-deprived breast cancer via modulation of the tumor microenvironment.Translational cancer research · 2026Article
- Review
- Designing the matrix: extracellular matrix-informed strategies for bioengineered cancer models.Frontiers in bioengineering and biotechnology · 2026Review
- GAB2 regulates lipid metabolism by activating the MEK/ERK/c-Myc pathway: impact on renal cell carcinoma progression.European journal of medical research · 2025Article
- Multimode MALDI-MSI deciphers matrine-induced metabolic reprogramming in prostate cancer xenografts: spatial mapping of low-molecular-weight compound alterations.Frontiers in pharmacology · 2025Article
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10 authors.
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Abstract
Antiandrogen therapies are effectively used to treat advanced prostate cancer, but eventually cancer adaptation drives unresolved metastatic castration-resistant prostate cancer (mCRPC). Adipose tissue influences metabolic reprogramming in cancer and was proposed as a contributor to therapy resistance. Using extracellular matrix (ECM)-mimicking hydrogel coculture models of human adipocytes and prostate cancer cells, we show that adipocytes from subcutaneous or bone marrow fat have dissimilar responses under the antiandrogen Enzalutamide. We demonstrate that androgen receptor (AR)-dependent cancer cells (LNCaP) are more influenced by human adipocytes than AR-independent cells (C4-2B), with altered lipid metabolism and adipokine secretion. This response changes under Enzalutamide, with increased AR expression and adipogenic and lipogenic genes in cancer cells and decreased lipid content and gene dysregulation associated with insulin resistance in adipocytes. This is in line with the metabolic syndrome that men with mCRPC under Enzalutamide experience. The all-human, all-3D, models presented here provide a significant advance to dissect the role of fat in therapy response for mCRPC.
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