Insights Into Infections and Inflammation in Prostate Cancer Development and Management: An Overview
TL;DR
A more comprehensive understanding of the interactions between infection, chronic inflammation, and PCa development may facilitate the identification of novel biomarkers and therapeutic targets and contribute to improved risk stratification, earlier detection, and more effective treatment of PCa.
Abstract
Prostate cancer (PCa) represents a major public health concern and continues to be one of the leading causes of cancer‐related mortality among men worldwide. Current epidemiological projections suggest that the incidence and associated burden of PCa are likely to increase, emphasizing the importance of advancing preventive measures, improving early diagnostic approaches, and refining targeted therapeutic strategies. While established risk factors, including age, genetic predisposition, lifestyle‐related factors, ethnicity, and androgen signaling, have been extensively studied, these factors alone do not fully explain the observed patterns of PCa development. Increasing evidence suggests that infection‐associated chronic inflammation plays a central role in prostate tumor initiation and progression. Chronic inflammation of the prostate, arising from conditions such as prostatitis, benign prostatic hyperplasia (BPH), lower urinary tract infections (UTIs), sexually transmitted infections (STIs), and prolonged or repeated catheterization, has been associated with histological and molecular changes that may predispose prostate tissue to malignant transformation. Moreover, emerging evidence suggests that alterations in the prostate microbiome may sustain inflammatory signaling, thereby influencing tumor initiation and progression. This review synthesizes current epidemiological findings and experimental evidence linking infection‐associated inflammation to the development of PCa. Particular focus is placed on inflammatory signaling pathways implicated in prostate tumorigenesis, including nuclear factor kappa B (NF‐κB), signal transducer and activator of transcription 3 (STAT3), cyclooxygenase‐2/prostaglandin E2 (COX‐2/PGE2), interleukin‐6 and interleukin‐8 signaling, Toll‐like receptor (TLR) pathways, and activation of the NLRP3 inflammasome. In addition, we discuss therapeutic strategies that are aimed at modulating these pathways and their potential relevance in PCa management. A more comprehensive understanding of the interactions between infection, chronic inflammation, and PCa development may facilitate the identification of novel biomarkers and therapeutic targets. Such advances could ultimately contribute to improved risk stratification, earlier detection, and more effective treatment of PCa.