ArticleFrontiers in pharmacology2026
PRDX1 promotes clear cell renal cell carcinoma progression by modulating EGFR-dependent AKT pathway activation.
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Renal cell carcinoma (RCC) is a highly heterogeneous malignant tumor, characterized by a globally increasing incidence and mortality rate. Although surgical resection serves as the standard treatment for localized RCC, recurrence and metastasis remain major clinical challenges. Based on patient sample analysis and signaling pathway investigation, the present study identifies peroxiredoxin 1 (PRDX1) as a potential therapeutic target for RCC. Methods: Patient microarray analysis, combined with data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases, revealed the expression pattern of PRDX1 in clear cell renal cell carcinoma (ccRCC) and confirmed its prognostic and diagnostic significance. Cell proliferation was evaluated using Cell Counting Kit-8 (CCK-8) assay, while cell motility was assessed via wound healing and transwell assays. Gene expression profiles and signaling pathways were analyzed through bioinformatics approaches including Western blot, immunohistochemistry and immunoprecipitation. A xenograft mouse model was utilized to investigate the Results: The analysis of 90 pairs of ccRCC samples demonstrated that elevated PRDX1 expression was significantly associated with higher malignancy in ccRCC and correlated with tumor prognosis and clinical stage. Comprehensive bioinformatics analysis identified a close relationship between PRDX1 inhibition and relative epidermal growth factor receptor (EGFR) pathways. Mechanistically, co-immunoprecipitation (Co-IP) assays revealed that PRDX1 could act as a molecular chaperone by binding to the juxta-membrane (JM) domain of EGFR to induce EGFR phosphorylation. The downregulation of PRDX1 significantly reduced their proliferation and migration capacities in renal cell lines ACHN and 786-O, whereas PRDX1 overexpression exerted the opposite effect. Importantly, the inhibitory effects of PRDX1 knockdown on ccRCC could be attenuated by EGF activation Conclusion: In summary, the findings of this study revealed a novel role of PRDX1 in triggering ccRCC progression by inducing the phosphorylation of EGFR, supporting that PRDX1 may serve as a potential therapeutic target for the clinical management of ccRCC.
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