Hsp27 inhibits release of mitochondrial protein Smac in multiple myeloma cells and confers dexamethasone resistance

Blood. 2003 Nov 1;102(9):3379-86. doi: 10.1182/blood-2003-05-1417. Epub 2003 Jul 10.

Abstract

Smac, second mitochondria-derived activator of caspases, promotes apoptosis via activation of caspases. Heat shock protein 27 (Hsp27) negatively regulates another mitochondrial protein, cytochrome c, during apoptosis; however, the role of Hsp27 in modulating Smac release is unknown. Here we show that Hsp27 is overexpressed in both dexamethasone (Dex)-resistant multiple myeloma (MM) cell lines (MM.1R, U266, RPMI-8226) and primary patient cells. Blocking Hsp27 by an antisense (AS) strategy restores the apoptotic response to Dex in Dex-resistant MM cells by triggering the release of mitochondrial protein Smac, followed by activation of caspase-9 and caspase-3. Moreover, AS-Hsp27 overcomes interleukin-6 (IL-6)-mediated protection against Dex-induced apoptosis. These data demonstrate that Hsp27 inhibits the release of Smac, and thereby confers Dex resistance in MM cells.

MeSH terms

  • Apoptosis / drug effects
  • Caspase 3
  • Caspase 9
  • Caspases / metabolism
  • Cell Line, Tumor
  • Dexamethasone / pharmacology*
  • Drug Resistance, Neoplasm*
  • HSP27 Heat-Shock Proteins
  • Heat-Shock Proteins / physiology*
  • Humans
  • Immunomagnetic Separation
  • Interleukin-6 / pharmacology
  • Molecular Chaperones
  • Multiple Myeloma / metabolism
  • Multiple Myeloma / pathology*
  • Neoplasm Proteins / physiology
  • Oligonucleotides, Antisense / pharmacology
  • Tumor Cells, Cultured

Substances

  • HSP27 Heat-Shock Proteins
  • HSPB1 protein, human
  • Heat-Shock Proteins
  • Interleukin-6
  • Molecular Chaperones
  • Neoplasm Proteins
  • Oligonucleotides, Antisense
  • Dexamethasone
  • CASP3 protein, human
  • CASP9 protein, human
  • Caspase 3
  • Caspase 9
  • Caspases