ArticleOncogene2026
PRR15 suppresses renal cell carcinoma progression via the NF-κB/FDX1 axis to induce cuproptosis and mitochondrial dysfunction.
Article in Oncogene, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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14 authors.
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Abstract
Cuproptosis is involved in the proliferation, metastasis, and drug resistance formation development of renal cell carcinoma (RCC) by regulating lipid metabolism and oxidative stress levels in the tumor microenvironment, with Ferredoxin 1 (FDX1) as a core regulator. Proline-rich 15 (PRR15) is a proline-rich protein, that we previously found to inhibit the malignant progression of triple-negative breast cancer through the regulation of the phosphatidylinositol 3-kinase (PI3K) pathway and epithelial-mesenchymal transition (EMT) pathway. However, the role of PRR15 in cuproptosis and its molecular mechanisms remain unknown. This study found confirmed that PRR15 promotes cuproptosis and mitochondrial damage in RCC cells and inhibits tumor proliferation and metastasis, as demonstrated in vivo and in vitro. When RCC develops, PRR15 silencing activates the nuclear factor kappa-B (NF-κB) signaling pathway, which inhibits FDX1 expression, ultimately blocking the cuproptosis process and increasing tumor invasiveness. Conversely, overexpression of PRR15 reverses this phenotype. This study reveals for the first time the regulatory mechanism of the PRR15/NF-κB/FDX1 axis in cuproptosis in RCC, providing a new strategy for the treatment of RCC patients.
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