Expression patterns and prognostic value of RUNX genes in kidney cancer

Ke Gao1,2,3, Fang Zhang4, Ke Chen5

  • 1Department of Anesthesia, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710004, China.

Scientific Reports
|July 23, 2021
PubMed

Insights

RUNX1 and RUNX3 are upregulated in kidney renal clear cell carcinoma (KIRC). High RUNX1 expression and low RUNX1 promoter methylation correlate with poor survival in KIRC patients, suggesting RUNX1 as a therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Kidney cancer, particularly kidney renal clear cell carcinoma (KIRC), is a significant urinary system malignancy.
  • Runt-related transcription factors (RUNX) play crucial roles in cellular functions, but their specific roles in kidney cancer require further investigation.

Purpose of the Study:

  • To elucidate the expression patterns and prognostic significance of RUNX genes in kidney cancer.
  • To investigate the potential of RUNX1 as a therapeutic target and its promoter methylation as a diagnostic/prognostic biomarker in KIRC.

Main Methods:

  • Utilized Oncomine, GEPIA, UALCAN, Kaplan-Meier Plotter, cBioPortal, and LinkedOmics to analyze DNA methylation, transcriptional, and survival data.
  • Compared RUNX gene expression and methylation levels between KIRC tissues and normal tissues.
  • Correlated RUNX1 expression and methylation with overall survival (OS) in KIRC patients.

Main Results:

  • RUNX1 and RUNX3 were found to be upregulated in KIRC tissues compared to normal tissues.
  • Higher RUNX1 transcription levels were significantly associated with poorer overall survival in KIRC patients.
  • KIRC tumor tissues exhibited lower RUNX1 promoter methylation levels, which correlated with decreased OS.

Conclusions:

  • RUNX1 emerges as a potential therapeutic target for KIRC treatment.
  • RUNX1 promoter methylation levels show promise as a novel diagnostic and prognostic biomarker for KIRC.
  • These findings provide a foundation for further research into RUNX1's role in KIRC.

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