ArticleNature communications2025
AR
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
15 citing papers in PubMed.
- Tumor‑immune spatiotemporal co‑evolution: A new paradigm for understanding and overcoming therapy resistance in metastatic castration‑resistant prostate cancer (Review).International journal of molecular medicine · 2026Review
- Pyrroline-5-carboxylate reductase 1 interacts with Nudix hydrolase 5 to drive bladder cancer malignant progression via activation of the APOE/JAK2/STAT3 signalling axis.Clinical and translational medicine · 2026Article
- Androgen receptor drives lenvatinib resistance in hepatocellular carcinoma through transcriptional activation of EIF3I and a downstream ceRNA axis.Oncology letters · 2026Article
- Hierarchical Targeting of TREM2Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Phase Separation of NFIB Suppresses SLC3A2-Mediated Ferroptosis in Castration-Resistant Prostate Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- HIF1 inhibition targets tumoral and myeloid cells, and is a promising therapy for metastatic castration-resistant prostate cancer.Cell death & disease · 2026Article
- The Multifaceted Role of Androgen Receptor Signaling in Immunity: Implications for Oncology.Molecular cancer research : MCR · 2026Review
- Review
- Targeted protein degradation dismantles undruggable targets to reverse immune evasion and therapy resistance in cancer.Frontiers in immunology · 2026Review
- Metabolic-Immune Coupling in Urologic Cancers: Macrophage Reprogramming as a Therapeutic Nexus.International journal of biological sciences · 2026Review
- Tumor-associated macrophages in cancer: from mechanisms to application.Molecular biomedicine · 2025Review
- TREM2-mediated regulation of myeloid cells in the tumor microenvironment: new insights and therapeutic prospects.NPJ precision oncology · 2025Review
- Positive and negative roles of myeloid cells in cancer immunotherapy.Journal for immunotherapy of cancer · 2025Review
- Shaping the macrophage landscape in the tumour microenvironment.Central-European journal of immunology · 2025Article
- TAM Plasticity under androgen deprivation therapy and PARP inhibition in prostate cancer: a multi-omics perspective.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
The androgen receptor (AR) usually drives prostate cancer cell growth, yet its role in immune cells such as tumour-associated macrophages (TAMs), remains unclear. We find that macrophages co-expressing AR and triggering receptor expressed on myeloid cells-2 (TREM2) exhibiting potent immunosuppressive and tumour-promoting effects. Genetic ablation of TREM2 combined with pharmacological blockade of AR, significantly reduces tumour progression in prostate cancer mouse models. Mechanistically, apolipoprotein E (APOE) in tumour microenvironment (TME) binds to TREM2 on macrophages and promotes AR expression. AR further upregulates transcription expression of Il10, Tgfb1, Il23a, and Ccl2 in macrophages. AR, TREM2, and APOE expression increases in prostate cancer patients and correlates with poor prognosis. In conclusion, these findings indicate an alternative mechanism of tumour immune evasion, supporting the development of immunomodulatory agents targeting AR and TREM2 in TAMs to delay or reverse endocrine therapy resistance or immune checkpoint therapy resistance in prostate cancer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.