HDAC4 degradation by combined TRAIL and valproic acid treatment induces apoptotic cell death of TRAIL-resistant head and neck cancer cells

Sci Rep. 2018 Aug 21;8(1):12520. doi: 10.1038/s41598-018-31039-8.

Abstract

Although TRAIL can directly induce cell death in some cancer cells, it appears that TRAIL resistance exists in many cancers. This study focuses on anti-cancer drugs for TRAIL-resistant head and neck cancer (HNC) to provide further progress toward effective cancer therapy. Results indicate in TRAIL-resistant HNC cells, that combined TRAIL and VPA treatment greatly reduced cell viability and therefore induced cell death, relative to treatment with TRAIL or VPA alone. A caspase-dependent signaling pathway was demonstrated, and combined treatment with TRAIL and VPA also significantly decreased the expression of HDAC4. When we pretreated cells with z-VAD followed by combined treatment with TRAIL and VPA, cell death was blocked with no reduction in expression of HDAC4. To confirm that cell death involved HDAC4 in HNC cells, we knocked down expression of HDAC4 with siRNA, followed by treatment with TRAIL and VPA. Results showed that loss of HDAC4 sensitized the TRAIL-resistant HNC cells to apoptotic cell death. Finally, we showed elevated expression of HDAC4 in HNC tissues compared to normal tissues obtained from the same patients. In conclusion, we suggest that combined VPA and TRAIL treatment may be a promising therapy for HNC via HDAC4 degradation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Caspases / metabolism
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Cell Survival / drug effects
  • Drug Resistance, Neoplasm / drug effects*
  • Drug Synergism
  • Gene Expression Regulation, Neoplastic / drug effects
  • Gene Knockdown Techniques
  • Head and Neck Neoplasms / drug therapy*
  • Head and Neck Neoplasms / genetics
  • Head and Neck Neoplasms / metabolism
  • Histone Deacetylases / chemistry*
  • Histone Deacetylases / genetics
  • Humans
  • Proteolysis
  • Repressor Proteins / chemistry*
  • Repressor Proteins / genetics
  • Signal Transduction / drug effects
  • TNF-Related Apoptosis-Inducing Ligand / pharmacology*
  • Up-Regulation / drug effects
  • Valproic Acid / pharmacology*

Substances

  • Repressor Proteins
  • TNF-Related Apoptosis-Inducing Ligand
  • Valproic Acid
  • Caspases
  • HDAC4 protein, human
  • Histone Deacetylases