Overload of the heat-shock protein H11/HspB8 triggers melanoma cell apoptosis through activation of transforming growth factor-beta-activated kinase 1

Oncogene. 2007 May 24;26(24):3521-31. doi: 10.1038/sj.onc.1210145. Epub 2006 Dec 18.

Abstract

Molecular therapeutics is a recognized promising approach for melanoma, but relevant target genes remain elusive. We report that overload of the recently cloned H11/HspB8 induces apoptosis in 55% of examined melanoma cultures. Apoptosis was determined by activation of caspases-9 and -3 and terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling (TUNEL), and was not seen in normal melanocytes. It was associated with H11/HspB8 complexation with transforming growth factor-beta-activated kinase (TAK) 1 and activation of TAK1 and p38 mitogen activated protein 3 kinases. TAK1 was not bound, nor activated by the H11/HspB8 mutant W51C, which has dominant antiapoptotic activity. beta-Catenin was phosphorylated by activated TAK1, inhibiting its nuclear accumulation and mictophthalmia-associated transcription factor and cyclin dependent kinase 2 expression. The dominant-negative TAK1 mutant K63W inhibited beta-catenin phosphorylation and caspase activation. The data indicate that H11/HspB8 overload causes melanoma growth arrest and apoptosis through TAK1 activation and suggest that H11/HspB8 is a promising molecular therapy target.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Apoptosis / drug effects
  • Apoptosis / physiology*
  • Caspases / drug effects
  • Caspases / metabolism
  • Cell Nucleus / metabolism
  • Cyclin-Dependent Kinase 2 / drug effects
  • Cyclin-Dependent Kinase 2 / metabolism
  • Doxorubicin / pharmacology
  • Enzyme Activation
  • Heat-Shock Proteins / genetics
  • Heat-Shock Proteins / metabolism*
  • Humans
  • MAP Kinase Kinase Kinases / metabolism*
  • Melanocytes / metabolism
  • Melanocytes / pathology
  • Melanoma / genetics
  • Melanoma / pathology*
  • Microphthalmia-Associated Transcription Factor / drug effects
  • Microphthalmia-Associated Transcription Factor / metabolism
  • Molecular Chaperones
  • Phosphorylation
  • Protein Serine-Threonine Kinases / genetics
  • Protein Serine-Threonine Kinases / metabolism*
  • Tumor Cells, Cultured
  • beta Catenin / drug effects
  • beta Catenin / metabolism
  • p38 Mitogen-Activated Protein Kinases / metabolism

Substances

  • HSPB8 protein, human
  • Heat-Shock Proteins
  • MITF protein, human
  • Microphthalmia-Associated Transcription Factor
  • Molecular Chaperones
  • beta Catenin
  • Doxorubicin
  • Protein Serine-Threonine Kinases
  • CDK2 protein, human
  • Cyclin-Dependent Kinase 2
  • p38 Mitogen-Activated Protein Kinases
  • MAP Kinase Kinase Kinases
  • MAP kinase kinase kinase 7
  • Caspases