Caspase-6 Induces 7A6 Antigen Localization to Mitochondria During FAS-induced Apoptosis of Jurkat Cells

Anticancer Res. 2017 Apr;37(4):1697-1704. doi: 10.21873/anticanres.11501.

Abstract

Background: Mitochondria are central to apoptosis. However, apoptosis progression involving mitochondria is not fully understood. A factor involved in mitochondria-mediated apoptosis is 7A6 antigen. 7A6 localizes to mitochondria from the cytosol during apoptosis, which seems to involve 'effector' caspases. In this study, we investigated the precise role of effector caspases in 7A6 localization to mitochondria during apoptosis.

Materials and methods: Human T-cell lymphoma Jurkat cells were treated with an antibody against FAS. 7A6 localization was analyzed by confocal laser scanning microscopy and flow cytometry. Caspases activation was determined by western blot analysis.

Results: 7A6 localization to mitochondria during anti-FAS-induced apoptosis was significantly reduced by the caspase-6 inhibitor, N-acetyl-Val-Glu-Ile-Asp-aldehyde, but not by the caspase-3 inhibitor, N-acetyl-Asp-Asn-Leu-Asp-aldehyde, nor caspase-7/3 inhibitor, N-acetyl-Asp-Gln-Thr-Asp-aldehyde. Moreover, caspase-6 down-regulation suppressed 7A6 localization to mitochondria.

Conclusion: Caspase-6 regulates 7A6 localization to mitochondria during anti-FAS-induced apoptosis of Jurkat cells.

Keywords: 7A6 antigen; Apo2.7; Apoptosis; caspase-6.

MeSH terms

  • Apoptosis / drug effects*
  • Blotting, Western
  • Caspase 6 / pharmacology*
  • Caspase Inhibitors / pharmacology
  • Flow Cytometry
  • Humans
  • Jurkat Cells
  • Membrane Proteins / metabolism*
  • Mitochondria / drug effects
  • Mitochondria / metabolism
  • Mitochondria / pathology*
  • fas Receptor / metabolism*

Substances

  • Caspase Inhibitors
  • FAS protein, human
  • Membrane Proteins
  • antigen 7A6
  • fas Receptor
  • Caspase 6