Related Experiment Video

Updated: Jun 28, 2025

Comparing Metastatic Clear Cell Renal Cell Carcinoma Model Established in Mouse Kidney and on Chicken Chorioallantoic Membrane
05:36

Comparing Metastatic Clear Cell Renal Cell Carcinoma Model Established in Mouse Kidney and on Chicken Chorioallantoic Membrane

Published on: February 8, 2020

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Epigenetic regulation of FOXI2 promotes clear cell renal cell carcinoma progression

Shuai Zhou1,2, Cong Cheng1,2, Yi Xiang Liao1,2

  • 1Department of Urology, Jing Zhou Hospital Affiliated to Yangtze University, PR China.

Heliyon
|April 17, 2024
PubMed

Insights

FOXI2 is downregulated and hypermethylated in clear cell renal cell carcinoma (ccRCC), inhibiting cancer cell proliferation. Its overexpression induces cell cycle arrest, offering potential epigenetic therapy strategies for ccRCC.

Area of Science:

  • Epigenetics
  • Oncology
  • Molecular Biology

Background:

  • Epigenetic alterations are crucial in tumorigenesis, offering therapeutic targets.
  • FOXI2, a transcription factor, has roles in development and disease, but its function in renal cell carcinoma is not well understood.

Purpose of the Study:

  • To investigate the role of FOXI2 in clear cell renal cell carcinoma (ccRCC) and chromophobe cell carcinoma (chRCC).
  • To explore the potential of FOXI2 as a prognostic marker and therapeutic target in ccRCC.

Main Methods:

  • Bioinformatics analysis of gene expression and methylation data.
  • Correlation analysis between FOXI2 levels and patient prognosis.
  • Gene enrichment analysis and in vitro cell function experiments (cell cycle, proliferation).

Main Results:

  • FOXI2 is significantly downregulated and hypermethylated in ccRCC, contrasting with chRCC.
  • FOXI2 expression correlates with better prognosis in ccRCC patients.
  • FOXI2 induces cell cycle arrest and inhibits cell proliferation in ccRCC cells.
  • Promoter hypermethylation regulates FOXI2 expression in ccRCC.

Conclusions:

  • FOXI2 acts as a tumor suppressor in ccRCC, with its downregulation driven by promoter hypermethylation.
  • FOXI2 warrants further investigation as a potential biomarker and therapeutic target for ccRCC.
Keywords:
Cell cycle arrestFOXI2MethylationRenal cancer

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