ArticleTranslational andrology and urology2026
Tea polyphenols suppress the malignant progression of renal cancer cells by targeting Nosip.
Article in Translational andrology and urology, 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 malignant tumor of the urinary system with a high incidence. Due to limited treatment options and poor prognosis, novel therapeutic strategies are urgently needed. Recent studies revealed that Nosip participates in cell growth regulation by activating endothelial nitric oxide synthase (eNOS) and mediating the ubiquitination of erythropoietin receptor, suggesting its potential role as an oncogene in RCC progression. Methods: Nosip expression was analyzed using reverse-transcription quantitative polymerase chain reaction (RT-qPCR) and Western blotting. Functional assays including Cell Counting Kit-8 (CCK-8), wound healing, Transwell, and apoptosis assays were performed to assess cell proliferation, migration, invasion, and apoptosis. Bioinformatics analysis was conducted using The Cancer Genome Atlas Kidney Clear Cell Carcinoma (TCGA-KIRC) dataset. Results: Nosip was significantly upregulated in RCC tissues and cells. Knockdown of Nosip inhibited RCC cell proliferation, migration, and invasion, while overexpression promoted these malignant phenotypes. Tea polyphenols (TPs) treatment suppressed RCC cell viability, induced apoptosis, and inhibited clonogenic capacity in a concentration-dependent manner. Mechanistically, TPs downregulated Nosip expression at both messenger RNA (mRNA) and protein levels. Rescue experiments demonstrated that Nosip overexpression attenuated, while Nosip knockdown enhanced, the anti-tumor effects of TPs. Conclusions: This study identifies Nosip as a proto-oncogene in RCC and demonstrates that TPs suppress RCC progression by directly targeting and downregulating Nosip. These findings establish Nosip as a potential therapeutic target and provide a mechanistic basis for developing TPs as a Nosip-targeted therapy for RCC.
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