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Review
. 2025 Jan 23;17(3):372.
doi: 10.3390/cancers17030372.

Periprostatic Adipose Tissue as a Contributor to Prostate Cancer Pathogenesis: A Narrative Review

Julia Drewa  1 , Katarzyna Lazar-Juszczak  2   3 , Jan Adamowicz  1   4 , Kajetan Juszczak  1
Affiliations
Review

Periprostatic Adipose Tissue as a Contributor to Prostate Cancer Pathogenesis: A Narrative Review

Julia Drewa et al. Cancers (Basel). .

Abstract

Periprostatic adipose tissue (PPAT) contributes to the pathogenesis of prostate cancer. The purpose of this study was to review and summarize the literature on the role of PPAT in prostate cancer pathogenesis. Moreover, we evaluated the clinical implication of PPAT in patients with prostate cancer. We performed a scoping literature review of PubMed from January 2002 to November 2024. Search terms included "periprostatic adipose tissue", "adipokines", and "prostate cancer". Secondary search involved reference lists of eligible articles. The key criterion was to identify studies that included PPAT, adipokines, and their role in prostate cancer biology and clinical features. In total 225 publications were selected for inclusion in this review. The studies contained in publications allowed us to summarize the data on the pathogenesis of PPAT as a contributor to prostate cancer biology and its aggressiveness. The review also presents new research directions for PPAT as a new target for the treatment of prostate cancer. Based on the current review, it can be stated that PPAT plays an important role in prostate cancer pathogenesis. Moreover, PPAT seems to be a promising target point when it comes to finding new therapies in patients with more aggressive and/or advanced stages of prostate cancer.

Keywords: adipokines; obesity; pathogenesis; periprostatic adipose tissue; prostate cancer.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Obesity-associated pathomechanisms of prostate cancer development. PPAT—Periprostatic adipose tissue, IGF-1—Insulin-like growth factor-1, NK—Natural Killer, PCa—prostate cancer.
Figure 2
Figure 2
Adipokines released from PPAT affect prostate cancer development. CCR3—chemokine receptor 3, CCL7—chemokine ligand 7, IL-1—interleukin-1, IL-6—interleukin-6, TNF-α—tumor necrosis factor α, VEGF—vascular endothelial growth factor, IGF-1—Insulin-like growth factor-1, BMPs—Bone Morphogenetic Proteins, UCPs—mitochondrial uncoupling protein.
Figure 3
Figure 3
The multidirectional action of adipokines released by periprostatic adipose tissue (e.g., chemokines, cytokines, angiogenic factors, and other substances (e.g., leptin, adiponectin, IGF1, HIF-1α, etc.) in prostate cancer pathogenesis.
See this image and copyright information in PMC

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