Differentially expressed proteins of BPH with tissue inflammation based on proteomic techniques
Abstract
Objective: To explore the molecular mechanism of benign prostatic hyperplasia (BPH) complicated by tissue inflammation, to identify and analyze differentially expressed proteins from a proteomic perspective, and to provide a basis for elucidating the role mechanism of the inflammatory microenvironment in BPH progression and for seeking potential intervention targets. Methods: Sixty BPH surgical patients were included and divided into a simple BPH group (n = 30) and a BPH with tissue inflammation group (n = 30) based on histological inflammation scores. Label-free quantitative proteomic analysis was performed using liquid chromatography-tandem mass spectrometry (LC-MS/MS) to compare the expression patterns of differentially expressed proteins between the two groups. Bioinformatics tools were employed to perform functional enrichment analysis (GO, KEGG) and construct protein-protein interaction networks (STRING) for the differentially expressed proteins. Key proteins were selected and independently validated by Western blot. Results: A total of approximately 4900 proteins were identified. Compared with the simple BPH group, the BPH with inflammation group showed significant differences (P < 0.05, FDR < 0.05) in inflammation-related molecules (i.e., proteins primarily associated with initiating or modulating inflammatory processes; e.g., S100A8 upregulated by 3.45-fold, S100A9 upregulated by 3.22-fold, MMP9 upregulated by 3.10-fold, CCL2 upregulated by 2.98-fold) and prostate normal secretion-related proteins (e.g., MSMB downregulated to 0.12-fold, ACPP downregulated to 0.15-fold). Bioinformatic analysis showed significant enrichment of inflammation response, cell chemotaxis, ECM-receptor interaction, and Chemokine and Jak-STAT pathways. STRING analysis revealed a network distribution of key proteins, with most hub nodes concentrated in the core links of inflammation and immune regulation. Western blot validation results were consistent with the omics data, supporting the real existence and role of core proteins (i.e., proteins with high connectivity or central regulatory influence in the interaction network) in the pathological mechanism of BPH with inflammation. Conclusion: There are specific differentially expressed proteins in BPH with tissue inflammation, and the associated molecular networks jointly influence local microenvironment remodeling and the hyperplastic process. Elucidating the roles of these molecules and pathways helps improve our understanding of BPH pathogenesis and provides strong clues for precise diagnosis and the exploration of individualized therapeutic strategies.
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