A role for IFN-lambda1 in multiple myeloma B cell growth

Leukemia. 2008 Dec;22(12):2240-6. doi: 10.1038/leu.2008.263. Epub 2008 Oct 2.

Abstract

Multiple myeloma (MM) is a progressive disease that results from dysregulated proliferation of plasma cells. Although, causative factors such as genetic events and altered expression of anti-apoptotic factors have been described in a number of patients, the mechanistic details that drive myeloma development and continued growth of malignant cells remain largely undefined. Numerous growth factors, including interleukin (IL)-6, Insulin-like growth factor-1 and IL-10 have been shown to promote growth of MM cells suggesting a significant role for cytokines in this disease. Interferon (IFN)-lambda1 is a new member of the Class II cytokine family that, similar to IFN-alpha, has been shown to mediate viral immunity. In light of data supporting a role for cytokines in myeloma, we investigated the significance of IFN-lambda1 on myeloma cell biology. Our studies show for the first time that myeloma cells bind to soluble IFN-lambda1, and that IFN-lambda1 induces myeloma cell growth and protects against dexamethasone-induced cell death. Our data also show that IFN-lambda1 induces phosphorylation of STAT1, STAT3 and Erk. Taken together, our results suggest that IFN-lambda1 may regulate myeloma cell biology and could prove to be therapeutically important.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • B-Lymphocytes / immunology
  • B-Lymphocytes / metabolism*
  • B-Lymphocytes / pathology*
  • Cell Death / drug effects
  • Cell Death / immunology
  • Cell Division / drug effects
  • Cell Division / immunology
  • Cell Line, Tumor
  • Dexamethasone / pharmacology
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Glucocorticoids / pharmacology
  • Humans
  • Interferons
  • Interleukins / genetics
  • Interleukins / immunology
  • Interleukins / metabolism*
  • Multiple Myeloma / immunology
  • Multiple Myeloma / metabolism*
  • Multiple Myeloma / pathology*
  • Phosphorylation
  • STAT1 Transcription Factor / metabolism
  • STAT3 Transcription Factor / metabolism
  • Tumor Cells, Cultured

Substances

  • Glucocorticoids
  • interferon-lambda, human
  • Interleukins
  • STAT1 Transcription Factor
  • STAT1 protein, human
  • STAT3 Transcription Factor
  • STAT3 protein, human
  • Dexamethasone
  • Interferons
  • Extracellular Signal-Regulated MAP Kinases