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Hsf1 is required for the nuclear translocation of p53 tumor suppressor

Qiang Li1, Rebecca A Feldman, Vijayababu M Radhakrishnan

  • 1Department of Cell Biology and Anatomy, Arizona Cancer Center, University of Arizona, Tucson, AZ 85724-5024, USA.

Neoplasia (New York, N.Y.)
|September 25, 2008
PubMed

Insights

Heat shock factor 1 (Hsf1) is essential for the nuclear import and activation of the p53 tumor suppressor. This study reveals Hsf1

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • p53 tumor suppressor inactivation in human cancers often involves nuclear exclusion.
  • Mutant cell lines were generated to study p53 nuclear importation defects.

Purpose of the Study:

  • To investigate the role of heat shock factor 1 (Hsf1) in p53 nuclear import and activation.
  • To identify factors regulating p53 localization in response to cellular stress.

Main Methods:

  • Isolation and characterization of p53 nuclear import-deficient mutant cell lines (ALTR12, ALTR19, ALTR25).
  • Western blot analysis to assess Hsf1 expression and p53 localization.
  • Heat shock and chemical treatments to induce p53 nuclear import.
  • Gene silencing (siRNA) and gene complementation (exogenous Hsf1) to determine Hsf1's role.
  • Reporter assays to measure p53-mediated p21 activation.

Main Results:

  • ALTR12 cells exhibited impaired Hsp70 induction and lacked Hsf1 expression, correlating with defective p53 nuclear import.
  • Heat shock and azetidine failed to induce p53 nuclear localization in ALTR12 cells, unlike parental cells.
  • Hsf1 suppression reduced p53 nuclear import and p21 reporter activation.
  • Restoration of Hsf1 in ALTR12 cells rescued p53 nuclear importation.

Conclusions:

  • Heat shock factor 1 (Hsf1) is crucial for the nuclear translocation and activation of p53.
  • Heat shock factors are implicated in the regulation of p53 localization and function.
  • Defects in Hsf1 may contribute to p53 dysfunction in certain tumors.

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