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RanGTPase: a candidate for Myc-mediated cancer progression

Hiu-Fung Yuen1, Vignesh-Kumar Gunasekharan, Ka-Kui Chan

  • 1Center for Cancer Research and Cell Biology, Queen's University of Belfast, Belfast, BT9 7BL, UK.

Journal of the National Cancer Institute
|March 8, 2013
PubMed
Abstract

Insights

The v-myc myelocytomatosis viral oncogene homolog (Myc) drives cancer progression by increasing Ras-related nuclear protein (Ran) expression. Targeting Ran may be a therapeutic strategy for Myc-driven cancers.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Ras-related nuclear protein (Ran) is crucial for cancer cell survival and progression.
  • The precise molecular mechanisms underlying Ran's role in cancer are not fully understood.

Purpose of the Study:

  • To investigate the effect of v-myc myelocytomatosis viral oncogene homolog (Myc) on Ran expression.
  • To determine the impact of Myc and Ran on cancer cell behavior.
  • To analyze the clinical relevance of Myc and Ran expression in patient cohorts.

Main Methods:

  • Western blot, chromatin immunoprecipitation, and luciferase reporter assays to assess Myc-Ran interactions.
  • Soft-agar, cell adhesion, and invasion assays to evaluate cancer cell phenotypes.
  • Analysis of 14 patient cohorts (n=2430) for Myc-Ran correlation and survival association.

Main Results:

  • Myc directly binds to and activates the Ran promoter, upregulating Ran expression.
  • Overexpression of Myc or Ran correlates with increased breast cancer progression and metastasis.
  • Knockdown of Ran mitigates the pro-cancer effects of Myc overexpression.
  • A positive correlation between Myc and Ran expression was observed in breast and lung cancer specimens.
  • Ran expression levels predict survival outcomes in patients with high Myc expression.

Conclusions:

  • Ran is essential for Myc-driven cancer progression.
  • Ran represents a potential therapeutic target for breast and lung cancers driven by Myc.

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