TY  - EJOU
AU  - Wu, Yang 
AU  - Xu, Dong 
AU  - Shi, Run 
AU  - Zhan, Mingwei 
AU  - Xu, Shaohui 
AU  - Wang, Xin 
AU  - Zhang, Jianpeng 
AU  - Zhou, Zhaokai 
AU  - Wang, Weizhuo 
AU  - Wang, Yongjie 
AU  - Li, Minglun 
AU  - Xu, Zihao 
AU  - Su, Kaifeng 

TI  - Cancer-Associated Fibroblasts in Prostate Cancer: Unraveling Mechanisms and Therapeutic Implications
T2  - Oncology Research

PY  - 2026
VL  - 34
IS  - 2
SN  - 1555-3906

AB  - Prostate cancer (PCa) remains a major cause of cancer-related mortality in men, largely due to therapy resistance and metastatic progression. Increasing evidence highlights the tumor microenvironment (TME), particularly cancer-associated fibroblasts (CAFs), as a critical determinant of disease behavior. CAFs constitute a heterogeneous population originating from fibroblasts, mesenchymal stem cells, endothelial cells, epithelial cells undergoing epithelial–mesenchymal transition (EMT), and adipose tissue. Through dynamic crosstalk with tumor, immune, endothelial, and adipocyte compartments, CAFs orchestrate oncogenic processes including tumor proliferation, invasion, immune evasion, extracellular matrix remodeling, angiogenesis, and metabolic reprogramming. This review comprehensively summarizes the cellular origins, phenotypic and functional heterogeneity, and spatial distribution of CAFs within the prostate TME. We further elucidate the molecular mechanisms by which CAFs regulate PCa progression and therapeutic resistance, and critically evaluate emerging strategies to therapeutically target CAF-mediated signaling, metabolic, and immune pathways. By integrating recent advances from single-cell and spatial transcriptomics (ST), our objective is to provide a holistic framework for understanding CAF biology and to highlight potential avenues for stromal reprogramming as an adjunct to current PCa therapies.
KW  - Prostate cancer; cancer-associated fibroblasts; tumor microenvironment; therapy resistance

DO  - 10.32604/or.2025.073265