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Mutant p53 regulates Dicer through p63-dependent and -independent mechanisms to promote an invasive phenotype

Patricia A J Muller1, Antonio G Trinidad, Patrick T Caswell

  • 1From the Cancer Research UK Beatson Institute, Glasgow G61 1BD, Scotland, United Kingdom and.

The Journal of Biological Chemistry
|November 14, 2013
PubMed

Insights

Reduced microRNA (miR) processing by Dicer depletion enhances cell invasion and receptor activation. Mutant p53 down-regulates Dicer, linking it to metastasis and revealing novel p53 functions.

Area of Science:

  • Cellular Biology
  • Molecular Oncology
  • Cancer Metastasis Research

Background:

  • MicroRNAs (miRs) are crucial regulators of cellular responses.
  • Reduced miR processing or Dicer depletion is linked to increased metastatic potential.

Purpose of the Study:

  • To investigate the role of Dicer depletion in cell invasion.
  • To explore the relationship between mutant p53, TAp63, and Dicer expression.
  • To understand the mechanisms by which mutant p53 influences Dicer activity.

Main Methods:

  • Cellular invasion assays.
  • Analysis of growth factor receptor (Met, EGF receptor) recycling and activation.
  • Investigation of Dicer expression regulation by mutant p53 and TAp63.
  • Assessment of TAp63-dependent and -independent pathways.

Main Results:

  • Dicer depletion enhances cell invasive behavior and growth factor receptor activation.
  • Mutant p53 down-regulates Dicer expression via TAp63-dependent and -independent mechanisms.
  • Mutant p53 directly inhibits TAp63-mediated Dicer transcription.
  • Mutant p53 independently controls Dicer protein levels.

Conclusions:

  • A direct link exists between mutant p53, TAp63, and Dicer, contributing to mutant p53-driven metastasis.
  • Mutant p53 exhibits TAp63-independent functions in controlling Dicer activity.
  • These findings offer insights into the molecular mechanisms of cancer cell invasion and metastasis.
Keywords:
Cell InvasionCell MotilityCell ScatteringDicerMicroRNAMutant p53p63

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