Castration-resistant prostate cancer (CRPC) is still a major concern in men’s health, with 375,000 cancer deaths annually. Hypoxia, which is a marked characteristic of advanced solid tumors, has been suggested to induce prostate cancer towards CRPC, metastasis and treatment resistance. To evaluate the effect of hypoxia on prostate cancer, two and five cycles of hypoxia and reoxygenation were administered using 22Rv1 cell lines and denominated as 22Rv1-CI and 22Rv1-PCI, respectively. Cancer cell migration was promoted in 22Rv1-CI compared to controls, and the expression of COL13A1 was significantly up-regulated in 22Rv1-CI according to differentially expressed gene analysis of RNA sequencing among groups. Cancer cell migration was impeded in a wound healing assay after transfecting si-COL13A1. Moreover, the expression of COL13A1 was also higher in the cell line originating from bone metastatic prostate cancer compared to other cell lines. Using the open database GEO, we also confirmed that the expression of COL13A1 was higher in bone metastatic prostate cancer tissue than in localized prostate cancer tissue in patients. Therefore, COL13A1 may be closely related to the bony metastasis of prostate cancer, and our findings may provide valuable information on the pathophysiology of the metastatic niche induced by hypoxia in patients with CRPC.

Purpose: Overactive bladder (OAB) in men with bladder outlet obstruction (BOO) due to benign prostatic hyperplasia (BPH) represents a major therapeutic challenge, as symptoms often persist even after surgical relief of obstruction. The underlying molecular mechanisms, however, remain poorly defined. The aim of this study was to identify differentially expressed proteins in the urothelial tissues of patients with BOO-related OAB using a proteomic approach.Methods: Bladder urothelial tissues were obtained via cold-cup biopsy during transurethral resection of the prostate in patients with BPH. Patients were classified into OAB and non-OAB groups. Proteomic profiling was conducted using liquid chromatography–tandem mass spectrometry, followed by functional annotation and pathway enrichment analyses with the Ingenuity Pathway Analysis and Gene Ontology tools.Results: Proteomic analysis identified 1,510 proteins, of which 133 were differentially expressed proteins in patients with OAB compared with the non-OAB group. Dysregulated pathways included cytoskeletal remodeling, Rho GTPase signaling, serotonergic signaling, and immune responses. Structural proteins such as ACTA2, CFL2, MYLK, and PPP1R12B were markedly downregulated, whereas GNA13 and multiple inflammatory mediators were upregulated. Functional analysis confirmed the enrichment of neurotransmitter catabolic processes, immune responses, and impaired cell-cell contact, suggesting structural disorganization and aberrant epithelial signaling in the OAB group.Conclusions: BOO-related OAB is associated with distinct molecular disturbances in cytoskeletal organization, neurotransmitter pathways, and immune responses. These proteomic findings provide novel insights into disease pathophysiology and highlight potential molecular targets for biomarker discovery and therapeutic interventions.