Onconase induces caspase-independent cell death in chemoresistant neuroblastoma cells

Cancer Lett. 2007 May 18;250(1):107-16. doi: 10.1016/j.canlet.2006.09.018. Epub 2006 Nov 3.

Abstract

The efficacy of Onconase on the growth of a panel of chemosensitive and chemoresistant neuroblastoma cell lines was investigated. Onconase decreased cell viability of chemosensitive (IMR-32, UKF-NB-3) and chemoresistant neuroblastoma cell lines characterised by high expression of P-glycoprotein (P-gp) (UKF-NB-3(r)DOX(20)) or by high P-gp expression in combination with mutated p53 (UKF-NB-3(r)VCR(10), Be(2)-C), in a similar manner. Moreover, Onconase caused cell cycle block in G1 phase and induced caspase-independent cell death. Transmission electron microscope investigations suggested that Onconase-induced autophagy contributes to Onconase-induced cell death. Antitumour activity of Onconase against naïve and drug-resistant neuroblastoma xenografts was confirmed in animals.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • ATP Binding Cassette Transporter, Subfamily B, Member 1 / analysis
  • Animals
  • Antineoplastic Agents / pharmacology*
  • Caspases / metabolism*
  • Cell Cycle
  • Cell Death
  • Cell Survival / drug effects
  • Drug Resistance, Neoplasm*
  • Female
  • Humans
  • Mice
  • Mice, Nude
  • Neuroblastoma / drug therapy*
  • Neuroblastoma / pathology
  • Ribonucleases / pharmacology*
  • Tumor Cells, Cultured
  • Xenograft Model Antitumor Assays

Substances

  • ATP Binding Cassette Transporter, Subfamily B, Member 1
  • Antineoplastic Agents
  • Ribonucleases
  • Caspases
  • ranpirnase