ArticleCell communication and signaling : CCS2026
Periprostatic adipose tissue-derived adipokine profile in prostate cancer patients reveals two distinct molecular phenotypes linked to obesity-related comorbidities: multifaceted role of lipocalin-2.
Article in Cell communication and signaling : CCS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Targeting lipocalin-2 in atherosclerosis: biological functions, pathogenic mechanisms, and therapeutic potential.Frontiers in cardiovascular medicine · 2026Review
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Abstract
backgroundProstate cancer (PCa) is a hormone-dependent tumor and one of the most prevalent cancers in men worldwide. PCa progression is influenced by its interaction with the surrounding tumor microenvironment, highlighting the role of periprostatic adipose tissue (PPAT), which modulates PCa behavior through the secretion of bioactive molecules (e.g., adipokines). However, the influence of this complex cell communication, particularly under altered metabolic conditions, remains to be fully elucidated.
methodsWe performed multiomic/bioinformatic approaches integrating transcriptomic, proteomic, and metabolomic data from PPATs and their secretome and circulating/urinary of lipocalin-2 (LCN2) levels using a well-characterized cohort [75 PCa-patients vs. 22 control subjects with benign prostate hyperplasia (BPH)]. Different prostate cell models [normal-like (PNT2) and PCa cells (DU145/LNCaP/22Rv1/PC-3)] were used to test the role of the LCN2/SLC22A17 axis in PCa cell via multiple functional (proliferation/apoptosis/migration/invasion/colony-formation/tumorsphere assays), molecular (transcriptomic/phospho-proteomic/targeted inflammatory proteomics), and preclinical (in vivo xenograft) analyses. External validation was performed using TCGA, Grasso, and Taylor cohorts, alongside longitudinal proteomic data from patient-derived xenograft models.
resultsA signature of significantly dysregulated adipokines was identified in PPAT of PCa vs. BPH patients. Unsupervised clustering analyses revealed two distinct molecular phenotypes (T1/T2) with unique adipokine fingerprints associated with differential obesity-related comorbidities (BMI/diabetes/dyslipidemia), being LCN2 the only adipokine showing consistent dysregulation at the transcriptomic/proteomic levels. Functional experiments demonstrated that LCN2 and its receptor SLC22A17 exert context- and transformation state-dependent effects [i.e., in vitro LCN2 and SLC22A17 overexpression promoting migration capacity in normal-like cells, while suppressing aggressive phenotypes (proliferation/invasion/stemness) in malignant models; these findings being also confirmed on in vivo xenograft models]. SLC22A17 expression was progressively lost during PCa progression and associated with significantly poorer survival across multiple independent cohorts. Mechanistically, LCN2 modulated critical oncogenic and inflammatory pathways, including NF-κB, TGF-β, JAK/STAT, and inflammasome-related signaling, and showed obesity-specific associations with arachidonic acid and complement components in the PPAT secretome.
conclusionsThese results demonstrate a profound dysregulation of the PPAT-derived adipokine profile in PCa associated with obesity-related comorbidities, and reveal a paradoxical, stage- and context-dependent dual role of the LCN2/SLC22A17 axis as a key modulator of PPAT-PCa microenvironment interactions, with potential implications for inflammation, metabolic signaling, and tumor progression.
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