Etoposide induces apoptosis via the mitochondrial- and caspase-dependent pathways and in non-cancer stem cells in Panc-1 pancreatic cancer cells

Oncol Rep. 2013 Dec;30(6):2765-70. doi: 10.3892/or.2013.2767. Epub 2013 Oct 1.

Abstract

Pancreatic cancer is a highly aggressive malignant tumor. In the present study, we performed several methods, including CCK-8 assay, immunofluorescence technique, western blotting and flow cytometry, to determine the effects of VP16 (etoposide) on Panc-1 pancreatic cancer cells. The results demonstrated that VP16 inhibited the growth of and induced apoptosis in Panc-1 cells. Western blot analysis showed that VP16 inhibited the expression of Bcl-2 and enhanced the expression of Bax, caspases-3 and -9, cytochrome c and PARP. Notably, a strong inhibitory effect of VP16 on Panc-1 cells mainly occurred in non-CSCs. These data provide a new strategy for the therapy of pancreatic cancer.

MeSH terms

  • Apoptosis / drug effects*
  • Caspase 3 / biosynthesis
  • Caspase 9 / biosynthesis
  • Cell Line, Tumor
  • Cytochromes c / biosynthesis
  • Etoposide / administration & dosage*
  • Gene Expression Regulation, Neoplastic / drug effects
  • Humans
  • Mitochondria / drug effects*
  • Neoplastic Stem Cells / drug effects
  • Pancreatic Neoplasms / drug therapy*
  • Pancreatic Neoplasms / genetics
  • Pancreatic Neoplasms / pathology
  • Signal Transduction / drug effects
  • bcl-2-Associated X Protein

Substances

  • bcl-2-Associated X Protein
  • Etoposide
  • Cytochromes c
  • Caspase 3
  • Caspase 9