ArticleScientific reports2026
KIN17 facilitates the initiation and progression of renal tumor progression through the PI3K-AKT-mTOR pathway.
Article in Scientific reports, 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
KIN17, well known as a DNA and RNA binding protein, is highly involved in the regulation of tumorigenesis of diverse human cancers, but its function in the cancer progression and metastasis of Renal Cell Carcinoma (RCC) remains unclear. The aims of this study were to identify the role of KIN17 in RCC. We performed the study with the PI3K/mTOR inhibitor PF-04691502 in vivo and vitro, detected the tumor invasion and migration dysfunction by using Bioinformatics Analysis, IHC, Scratch Wound Healing Assay, Cell Viability Assay, Colony Formation Assays, EdU-647 Labeling, Cell Cycle and Apoptosis Detection by flow cytometer, Western Blotting, Animal Experiment. These findings suggest that the ability of KIN17 is to promote RCC cell proliferation, cycle progression, reduce cell apoptosis, increase cell clone formation, invasion, and increase cell migration and so on. As expected, PI3K/mTOR pathway inhibitor can reverse the ability of KIN17 in vivo and vitro. Meanwhile, PI3K/mTOR pathway inhibitor can reverse the activation of the PI3K/AKT/mTOR signaling pathway. Overall, our findings provide preliminary data which suggests KIN17 could be a promising migration and invasion prognostic biomarker, as well as a potential therapeutic target in RCC.
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