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Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter
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B-MYB-p53-related relevant regulator for the progression of clear cell renal cell carcinoma

M Nientiedt1, K Müller2, K Nitschke2

  • 1Department of Urology and Urosurgery, Medical Faculty Mannheim, University Medical Center Mannheim, University of Heidelberg, Theodor-Kutzer-Ufer 1-3, 68167, Mannheim, Germany. malin.nientiedt@umm.de.

Journal of Cancer Research and Clinical Oncology
|September 20, 2020
PubMed
Abstract

Insights

High B-MYB expression in clear cell renal cell carcinoma (ccRCC) correlates with advanced disease and poorer survival. This suggests B-MYB may be a therapeutic target in ccRCC, potentially bypassing normal p53 regulation.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Clear cell renal cell carcinoma (ccRCC) is the most common subtype of kidney cancer.
  • Understanding the molecular mechanisms driving ccRCC progression is crucial for developing effective therapies.

Purpose of the Study:

  • To investigate the mRNA expression of B-MYB and MDM2 in ccRCC.
  • To explore the relationship between B-MYB, MDM2, and p53 in ccRCC.
  • To assess the prognostic significance of B-MYB and MDM2 expression in ccRCC patients.

Main Methods:

  • Gene expression screening using the TCGA ccRCC cohort (529 patients).
  • Validation of mRNA expression via qRT-PCR in a separate ccRCC cohort (101 patients).
  • Statistical analysis including correlation studies and multivariable Cox regression for survival prediction.

Main Results:

  • B-MYB mRNA expression was significantly elevated in high-grade and advanced-stage ccRCC tumors in both cohorts.
  • Correlations between p53-B-MYB and MDM2-B-MYB were observed in low-grade ccRCC but diminished in high-grade/advanced tumors.
  • Upregulated B-MYB and downregulated MDM2 independently predicted poorer overall survival (OS) and progression-free survival (PFS) in the TCGA cohort, with partial confirmation in the validation cohort.

Conclusions:

  • High B-MYB expression is prevalent in advanced ccRCC and associated with adverse clinical outcomes.
  • The loss of B-MYB-p53 network correlation in advanced ccRCC suggests alternative oncogenic pathways.
  • B-MYB represents a potential therapeutic target for ccRCC, warranting further investigation into its signaling pathways.
Keywords:
Kidney cancerMDM2MYBL2Therapy targetTumour markerUpstream regulation

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