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PRR11 promotes ccRCC tumorigenesis by regulating E2F1 stability.

Siming Chen1, Zhiwen He1, Tianchen Peng1

  • 1Department of Urology and.

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|September 9, 2021
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Proline rich 11 (PRR11) acts as an oncogene in clear cell renal cell carcinoma (ccRCC). PRR11 promotes ccRCC progression by degrading E2F1 protein, and its expression is activated by c-Myc.

Keywords:
CancerCell BiologyCell cycleNephrology

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Proline rich 11 (PRR11) is implicated in various tumors.
  • The role of PRR11 in human clear cell renal cell carcinoma (ccRCC) remains unelucidated.

Purpose of the Study:

  • To investigate the biological functions and clinical significance of PRR11 in ccRCC.
  • To explore the molecular mechanisms underlying PRR11's role in ccRCC progression.

Main Methods:

  • Bioinformatic analysis to identify PRR11 as a ccRCC biomarker.
  • In vitro and in vivo experiments involving PRR11 silencing.
  • Protein interaction and stability assays to study PRR11-E2F1 interaction.
  • Analysis of c-Myc's regulation of PRR11 expression.

Main Results:

  • PRR11 was identified as a biomarker and predictor of poor prognosis in ccRCC.
  • PRR11 silencing inhibited ccRCC cell proliferation and migration.
  • PRR11 promotes ccRCC progression by inducing E2F1 degradation and reducing its stability, affecting cell cycle.
  • PRR11 is a target gene of c-Myc, which enhances PRR11 expression in ccRCC.

Conclusions:

  • PRR11 functions as an oncogene in ccRCC.
  • PRR11 negatively regulates E2F1 protein stability, contributing to ccRCC development.
  • c-Myc-mediated activation of PRR11 accelerates ccRCC progression.