Activity of suberoylanilide hydroxamic Acid against human breast cancer cells with amplification of her-2

Clin Cancer Res. 2005 Sep 1;11(17):6382-9. doi: 10.1158/1078-0432.CCR-05-0344.

Abstract

Purpose: We determined the effects of suberoylanilide hydroxamic acid (SAHA), a histone deacetylase inhibitor, on hsp90 and its client proteins Her-2, AKT, and c-Raf, as well as evaluated the cytotoxic effects of co-treatment of SAHA with trastuzumab or docetaxel in human breast cancer BT-474 and SKBR-3 cells containing amplification of Her-2.

Experimental design: The cells were treated with SAHA (1.0-5.0 micromol/L) and/or trastuzumab (5-40 microg/mL) or docetaxel (5-20 nmol/L). Following this, apoptosis and the levels of p21(WAF1), p27(KIP1), AKT, c-Raf, and Her-2, as well as of the key regulators of apoptosis were determined. Synergistic interaction between drugs was evaluated by median dose-effect analysis.

Results: Treatment with SAHA up-regulated p21(WAF1) and p27(KIP1) levels, increased the percentage of cells in G2-M phase of the cell cycle, as well as induced apoptosis in a dose-dependent manner. This was associated with up-regulation of the pro-death Bak and Bim, as well as with attenuation of the levels of Her-2 and XIAP, survivin, Bcl-2, and Bcl-x(L) proteins. SAHA treatment induced acetylation of hsp90. This reduced the chaperone association of Her-2 with hsp90, promoting polyubiquitylation and degradation of Her-2. SAHA also attenuated the levels of c-Raf and AKT. Co-treatment with SAHA significantly increased trastuzumab or docetaxel-induced apoptosis of BT-474 and SKBR-3 cells. Additionally, median dose-effect analysis revealed that co-treatment with SAHA and trastuzumab or docetaxel induced synergistic cytotoxic effects against the breast cancer cells.

Conclusions: These preclinical findings support the development of SAHA in combination with docetaxel and/or trastuzumab against Her-2-amplified breast cancer.

MeSH terms

  • Acetylation
  • Antibodies, Monoclonal / administration & dosage
  • Antibodies, Monoclonal, Humanized
  • Antineoplastic Combined Chemotherapy Protocols / pharmacology
  • Apoptosis / drug effects
  • Blotting, Western
  • Breast Neoplasms / drug therapy*
  • Breast Neoplasms / genetics
  • Cell Cycle Proteins / metabolism
  • Cell Division / drug effects
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclin-Dependent Kinase Inhibitor p27
  • Docetaxel
  • Drug Synergism
  • Flow Cytometry
  • G2 Phase / drug effects
  • Gene Amplification*
  • HSP90 Heat-Shock Proteins / metabolism
  • Histone Deacetylase Inhibitors
  • Humans
  • Hydroxamic Acids / pharmacology*
  • Inhibitor of Apoptosis Proteins
  • Microtubule-Associated Proteins / metabolism
  • Neoplasm Proteins / metabolism
  • Proteasome Endopeptidase Complex / drug effects
  • Protein Serine-Threonine Kinases / metabolism
  • Proteins / metabolism
  • Proto-Oncogene Proteins / metabolism
  • Proto-Oncogene Proteins c-akt
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Proto-Oncogene Proteins c-raf / metabolism
  • Receptor, ErbB-2 / genetics*
  • Receptor, ErbB-2 / metabolism
  • Signal Transduction / drug effects*
  • Survivin
  • Taxoids / administration & dosage
  • Trastuzumab
  • Tumor Cells, Cultured
  • Tumor Suppressor Proteins / metabolism
  • Vorinostat
  • X-Linked Inhibitor of Apoptosis Protein
  • bcl-X Protein

Substances

  • Antibodies, Monoclonal
  • Antibodies, Monoclonal, Humanized
  • BCL2L1 protein, human
  • BIRC5 protein, human
  • CDKN1A protein, human
  • Cell Cycle Proteins
  • Cyclin-Dependent Kinase Inhibitor p21
  • HSP90 Heat-Shock Proteins
  • Histone Deacetylase Inhibitors
  • Hydroxamic Acids
  • Inhibitor of Apoptosis Proteins
  • Microtubule-Associated Proteins
  • Neoplasm Proteins
  • Proteins
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • Survivin
  • Taxoids
  • Tumor Suppressor Proteins
  • X-Linked Inhibitor of Apoptosis Protein
  • XIAP protein, human
  • bcl-X Protein
  • Cyclin-Dependent Kinase Inhibitor p27
  • Docetaxel
  • Vorinostat
  • Receptor, ErbB-2
  • AKT1 protein, human
  • Protein Serine-Threonine Kinases
  • Proto-Oncogene Proteins c-akt
  • Proto-Oncogene Proteins c-raf
  • Proteasome Endopeptidase Complex
  • Trastuzumab