IL-18 enhances SCF production of melanoma cells by regulating ROI and p38 MAPK activity

Immunol Lett. 2005 Jan 31;96(2):211-7. doi: 10.1016/j.imlet.2004.08.008.

Abstract

It has been reported that interleukin-18 (IL-18) is secreted by B16 murine melanoma cells and that this endogenous IL-18 is involved in the immune escape of murine melanoma cells. The present study investigated whether interleukin (IL)-18 can regulate stem cell factor (SCF) expression, known to be associated with melanocyte proliferation, in B16F10 murine melanoma cells. SCF expression was examined by RT-PCR, intracellular FACS analysis, and ELISA in IL-18 antisense transfectants. Transfection with IL-18 antisense cDNA reduced SCF expression and the expression was enhanced by addition of exogenous IL-18. In addition, the effect of IL-18 was blocked by the antioxidant, N-acetyl-L-cysteine (NAC), indicating that IL-18 regulates ROI production, which is involved in SCF production. Furthermore, inhibitors of p38 mitogen-activated protein kinase (MAPK), such as SB203580, blocked enhanced SCF expression, indicating that p38 MAPK activity is required for IL-18-enhanced SCF production. Taken together, these results suggest that IL-18 plays a critical role as a regulatory factor of SCF expression via ROI and p38 MAPK activity in B16F10 murine melanoma cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line, Tumor
  • DNA, Antisense / genetics
  • DNA, Antisense / pharmacology
  • Enzyme Activation
  • Interleukin-18 / genetics
  • Interleukin-18 / pharmacology
  • Interleukin-18 / physiology*
  • Melanoma, Experimental / metabolism*
  • Mice
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Reactive Oxygen Species / metabolism*
  • Stem Cell Factor / biosynthesis*
  • Stem Cell Factor / genetics
  • p38 Mitogen-Activated Protein Kinases / metabolism*

Substances

  • DNA, Antisense
  • Interleukin-18
  • RNA, Messenger
  • Reactive Oxygen Species
  • Stem Cell Factor
  • p38 Mitogen-Activated Protein Kinases