Mda-7/IL-24 induces apoptosis of diverse cancer cell lines through JAK/STAT-independent pathways

J Cell Physiol. 2003 Aug;196(2):334-45. doi: 10.1002/jcp.10309.

Abstract

Experimental evidence documents that the MDA-7/IL-24 protein (an IL-10 family cytokine) binds to IL-20 and IL-22 receptor complexes resulting in the activation of JAK/STAT signaling pathways. Recent published reports utilizing human blood derived primary lymphocytes have provided additional confirmatory evidence relating to the cytokine properties of this molecule. A notable attribute of mda-7/IL-24 is its cancer cell-specific apoptosis inducing capacity, which currently remains incompletely understood. Treatment with distinctive tyrosine kinase inhibitors (Genistein and AG18) or a JAK-selective inhibitor (AG490) did not prevent Ad.mda-7 induced apoptosis in diverse cell lines. In addition, there is no apparent correlation between patterns of expression of IL-20R1, IL-20R2, and IL-22R mRNA and susceptibility to Ad.mda-7 in different cell lines. Furthermore, Ad.mda-7 is able to induce killing in STAT/JAK deficient cells. In contrast, treatment with the p38(MAPK) selective inhibitor SB203580, partially inhibited apoptosis induced by Ad.mda-7 in different cell lines. These results demonstrate for the first time that signaling events leading to susceptibility to Ad.mda-7 induced apoptosis, might be tyrosine kinase independent and can thus be distinguished from its cytokine function related properties mediated by the IL-20/IL-22 receptor complexes that require JAK/STAT kinase activity.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adenoviridae / genetics
  • Apoptosis*
  • Cell Line, Transformed
  • Drug Resistance
  • Enzyme Inhibitors / pharmacology
  • Gene Transfer Techniques
  • Genes, Tumor Suppressor
  • Genetic Vectors
  • HeLa Cells
  • Humans
  • Interleukins / genetics
  • Interleukins / metabolism*
  • Mitogen-Activated Protein Kinases / metabolism
  • Neoplasms / physiopathology*
  • Protein-Tyrosine Kinases / antagonists & inhibitors
  • Protein-Tyrosine Kinases / metabolism*
  • Receptors, Interleukin / metabolism
  • Trans-Activators / metabolism*
  • Tumor Cells, Cultured
  • p38 Mitogen-Activated Protein Kinases

Substances

  • Enzyme Inhibitors
  • Interleukins
  • Receptors, Interleukin
  • Trans-Activators
  • interleukin-22 receptor
  • interleukin-24
  • Protein-Tyrosine Kinases
  • Mitogen-Activated Protein Kinases
  • p38 Mitogen-Activated Protein Kinases
  • interleukin 20