ArticleBrazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica2025
Overexpression of SERPINA3 inhibits castration-resistant prostate cancer progression by enhancing M1 macrophage recruitment via CXCL2 upregulation.
Article in Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- The Serpin Superfamily in Adipose Tissue Remodeling: Molecular Drivers of Immune-Metabolic Crosstalk and Insulin Sensitivity.Biology · 2026Review
- Identification of novel protein markers and therapeutic targets for common urological cancers by integrating large-scale human plasma proteome with the genome.Scientific reports · 2026Article
- Graphene Far-Infrared Therapy Enhances Diabetic Wound Healing Through Potential Mitigation of Oxidative Stress and Inflammation and Regulation of Chemokines and Macrophage Polarization.International journal of molecular sciences · 2026Article
- Characterization of the tumor microenvironment in locally advanced gastric cancer and identification of spatially predictive biomarkers associated with beneficial neoadjuvant immunochemotherapy.Frontiers in immunology · 2026Article
- Sphingolipid Metabolism in the Pathogenesis of Hashimoto's Thyroiditis.International journal of molecular sciences · 2025Review
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Abstract
The primary objective of the present study was to identify differentially expressed genes (DEGs) associated with castration-resistant prostate cancer (CRPC) to verify the potential mechanism of CRPC progression. DEGs from CRPC datasets were filtered with a P<0.05 and Spearman correlation coefficient ≥0.3. Serpin peptidase inhibitor, clade A member 3 (SERPINA3), was uniquely present in three CRPC datasets, and its low expression in CRPC was confirmed in cell lines and tissues. Colony formation, transwell assays, and subcutaneous tumor formation experiments in mice demonstrated that overexpression of SERPINA3 may significantly inhibit the proliferation and invasion of PC3 cells. Mechanistic studies revealed that, in prostate cancer (PCa), SERPINA3 can activate the interleukin (IL)-17 and tumor necrosis factor (TNF)α signaling pathways by promoting the expression of CXC chemokine ligand 2 (CXCL2), thereby increasing the recruitment of M1 macrophages into the tumor microenvironment and inhibiting the progression of PCa. The current results indicated that the expression of SERPINA3 may be negatively correlated with CRPC, and it could promote the M1 polarization of macrophages and inhibit the progression of CRPC by increasing the expression of CXCL2.
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