ArticleFrontiers in immunology2026
Integrative multi-omics identifies PANX2 as a ferroptosis suppressor and potential therapeutic target in clear cell renal cell carcinoma.
Article in Frontiers in immunology, 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: Clear cell renal cell carcinoma (ccRCC) is metabolically primed for ferroptosis, yet the prognostic relevance and mechanistic contribution of ferroptosis-related genes remain incompletely defined. This study aimed to identify ferroptosis-associated biomarkers with prognostic value and to clarify their functional relevance in ccRCC progression. Methods: We integrated single-cell RNA sequencing, bulk RNA-seq, spatial transcriptomics, and machine-learning-based feature selection to identify ferroptosis-related prognostic genes in ccRCC. A four-gene risk model and an integrated nomogram were constructed and evaluated in independent cohorts. PANX2 was prioritized for experimental validation using stable knockdown models, RNA sequencing, lipid peroxidation and iron probes, redox assays, Western blot, luciferase reporter assays, xenografts, and an immunocompetent murine renal carcinoma model. Results: A four-gene prognostic signature (CA9, PVT1, RRM2, and PANX2) was identified and used to construct a risk model with consistent predictive performance in the training and external validation cohorts. Among these genes, PANX2 was predominantly enriched in epithelial tumor compartments and had not been functionally characterized in ccRCC. PANX2 knockdown inhibited ccRCC cell proliferation, reduced antioxidant capacity, increased intracellular Fe Conclusions: This study identifies PANX2 as a ccRCC-relevant suppressor of ferroptosis and supports the involvement of a PANX2-Akt/mTOR-SLC7A11-associated signaling axis in redox homeostasis and tumor progression. The ferroptosis-related prognostic model and nomogram may support risk stratification, while PANX2 represents a candidate therapeutic vulnerability that warrants further mechanistic and translational validation.
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