Related Experiment Video

Updated: Jan 21, 2026

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
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Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

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KIN17 facilitates the initiation and progression of renal tumor progression through the PI3K-AKT-mTOR pathway

Yibo Wen1, Lei Lyu1, He Zhang1

  • 1Henan Joint International Pediatric Urodynamic Laboratory and Department of Urology, Urodynamic Centre, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450000, China.

Scientific Reports
|January 19, 2026
PubMed

Insights

KIN17 promotes renal cell carcinoma (RCC) progression, invasion, and metastasis. Targeting the PI3K/AKT/mTOR pathway with inhibitors can reverse these effects, suggesting KIN17 as a therapeutic target for RCC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • The role of KIN17, a DNA and RNA binding protein, in renal cell carcinoma (RCC) progression and metastasis is not well understood.
  • KIN17 is implicated in the tumorigenesis of various human cancers.

Purpose of the Study:

  • To elucidate the function of KIN17 in RCC.
  • To investigate KIN17's role in cancer progression and metastasis.
  • To explore KIN17 as a potential therapeutic target in RCC.

Main Methods:

  • In vivo and in vitro studies using the PI3K/mTOR inhibitor PF-04691502.
  • Bioinformatics Analysis, Immunohistochemistry (IHC), Scratch Wound Healing Assay, Cell Viability Assay, Colony Formation Assays, EdU-647 Labeling.
  • Cell Cycle and Apoptosis Detection (flow cytometry), Western Blotting, and Animal Experiments were performed.

Main Results:

  • KIN17 promotes RCC cell proliferation, cell cycle progression, and colony formation.
  • KIN17 reduces cell apoptosis and enhances cell invasion and migration.
  • PI3K/mTOR pathway inhibition reversed KIN17's pro-tumorigenic effects in vitro and in vivo.
  • Inhibitor treatment also reversed the activation of the PI3K/AKT/mTOR signaling pathway.

Conclusions:

  • KIN17 promotes RCC progression, invasion, and metastasis.
  • KIN17 could serve as a prognostic biomarker for RCC migration and invasion.
  • Targeting KIN17, potentially via the PI3K/AKT/mTOR pathway, represents a promising therapeutic strategy for RCC.
Keywords:
KIN17PI3K/AKT/mTORPI3K/mTOR pathway inhibitorRenal clear cell carcinoma

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