Unveiling the missing link between chronic prostatitis and prostate cancer: emerging roles of exosomal miRNAs as extracellular vesicle messengers
Abstract
Chronic inflammation can remodel the prostatic tissue ecosystem and may increase susceptibility to prostate cancer (PCa); however, direct causal evidence linking chronic prostatitis (CP) to PCa is still lacking, and the mechanisms of sustained intercellular information transfer remain unclear. Exosomal miRNAs are stable, selectively packaged, and capable of multi-target regulation, enabling them to transmit inflammation-related signals among epithelial cells, immune cells, and stromal cells. Patients with CP, particularly chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS), and those with PCa both exhibit aberrant exosomal miRNA profiles, and some of these miRNAs are associated with inflammatory responses, oxidative stress, immune regulation, epithelial–mesenchymal transition (EMT), and tumor microenvironment remodeling. This review summarizes current evidence on exosomal miRNAs in CP and PCa and proposes a testable working hypothesis: CP-associated exosomal miRNAs may act as molecular information carriers linking chronic inflammation and PCa by sustaining inflammation, reprogramming cellular states, and remodeling the local microenvironment, thereby promoting the formation of a tumor-prone tissue ecosystem. We also evaluate their potential as risk-stratification biomarkers and therapeutic targets, and highlight that long-term cohort studies, cell-of-origin tracing, and direct functional validation are critical to testing this hypothesis. Elucidating this mechanism may provide a theoretical basis for early identification and precision intervention of inflammation-associated PCa.
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BibTeX
@article{shen2026unveiling,
title = {{Unveiling the missing link between chronic prostatitis and prostate cancer: emerging roles of exosomal miRNAs as extracellular vesicle messengers}},
author = {Yihang Shen and Baojun Ju},
journal = {Frontiers in Immunology},
year = {2026},
month = nov,
doi = {10.3389/fimmu.2026.1983898},
url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1983898},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Unveiling the missing link between chronic prostatitis and prostate cancer: emerging roles of exosomal miRNAs as extracellular vesicle messengers
AU - Yihang Shen
AU - Baojun Ju
PY - 2026
DA - 2026/11/03
JO - Frontiers in Immunology
DO - 10.3389/fimmu.2026.1983898
UR - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1983898
AB - Chronic inflammation can remodel the prostatic tissue ecosystem and may increase susceptibility to prostate cancer (PCa); however, direct causal evidence linking chronic prostatitis (CP) to PCa is still lacking, and the mechanisms of sustained intercellular information transfer remain unclear. Exosomal miRNAs are stable, selectively packaged, and capable of multi-target regulation, enabling them to transmit inflammation-related signals among epithelial cells, immune cells, and stromal cells. Patients with CP, particularly chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS), and those with PCa both exhibit aberrant exosomal miRNA profiles, and some of these miRNAs are associated with inflammatory responses, oxidative stress, immune regulation, epithelial–mesenchymal transition (EMT), and tumor microenvironment remodeling. This review summarizes current evidence on exosomal miRNAs in CP and PCa and proposes a testable working hypothesis: CP-associated exosomal miRNAs may act as molecular information carriers linking chronic inflammation and PCa by sustaining inflammation, reprogramming cellular states, and remodeling the local microenvironment, thereby promoting the formation of a tumor-prone tissue ecosystem. We also evaluate their potential as risk-stratification biomarkers and therapeutic targets, and highlight that long-term cohort studies, cell-of-origin tracing, and direct functional validation are critical to testing this hypothesis. Elucidating this mechanism may provide a theoretical basis for early identification and precision intervention of inflammation-associated PCa.
SN - 1664-3224
ER -