ReviewFrontiers in immunology2025
IL-6/STAT3 signaling in prostate cancer: CAF-driven immune evasion and therapeutic opportunities.
Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 5 papers.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- Tumour-macrophage crosstalk initiated by NFIC/METTL3 negative feedback loop via exosomal miR-194-5p promotes NSCLC progression.Clinical and translational medicine · 2026Article
- Endocrine-driven inflammatory-epigenetic adaptation as a proposed axis of radioresistance in endocrine-exposed prostate cancer: a translational hypothesis.Frontiers in endocrinology · 2026Review
- Tumor-associated macrophages and lineage plasticity in prostate cancer: from established myeloid programs to emerging spatial hypotheses.Frontiers in immunology · 2026Review
- Tumor-immune spatiotemporal co-evolution as a paradigm for overcoming therapy resistance in advanced prostate cancer.Frontiers in immunology · 2026Review
- CALB2 mediates tumor progression and immune escape in colorectal cancer by shaping an inhibitory immune microenvironment.Frontiers in immunology · 2026Article
Corrections and comments
- Erratum issued
Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin-6 (IL-6) plays a pivotal regulatory role in prostate cancer progression, contributing to therapy resistance and reshaping of the tumor microenvironment. This review outlines the clinical relevance of IL-6 as a potential prognostic biomarker and describes its mechanistic involvement in the development of castration resistance, with emphasis on its interplay with distinct cancer-associated fibroblast (CAF) subtypes. Elevated serum IL-6 levels in metastatic castration-resistant prostate cancer are associated with poor responses to docetaxel, enzalutamide, or abiraterone, and correlate with worse prognosis. Mechanistically, IL-6 promotes neuroendocrine differentiation and sustains cell survival under therapeutic stress through activation of signal transducer and activator of transcription 3 (STAT3), mitogen-activated protein kinase (MAPK), and androgen receptor signaling pathways. Recent single-cell studies reveal that prostate CAFs are highly heterogeneous. Certain subtypes are linked to extracellular matrix remodeling and fibrosis, while others exhibit inflammatory or immune-modulatory characteristics, differentially influencing tumor evolution. Specific CAF subsets have been strongly implicated in promoting castration resistance and adverse outcomes. Therapeutic strategies targeting the IL-6/IL-6R axis-such as neutralizing antibodies, advanced chimeric antigen receptor (CAR)-T designs, and combination regimens-are under active investigation. Simultaneously, modulating CAF plasticity to convert tumor-promoting phenotypes into tumor-restraining ones represents a promising therapeutic avenue. A deeper understanding of IL-6 functions across CAF subtypes may unlock novel precision therapy opportunities for prostate cancer.
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What Socratic holds
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 Socratic graph.