Autocrine interleukin-6/interleukin-6 receptor stimulation in non-small-cell lung cancer

Clin Lung Cancer. 2006 Jan;7(4):273-5. doi: 10.3816/CLC.2006.n.006.

Abstract

Autocrine growth factor stimulation resulting in growth self-sufficiency is a hallmark of cancer. Classically, non-small-cell lung cancer (NSCLC) cells have autocrine epidermal growth factor stimulation through coexpression of receptors and ligands. In addition to epidermal growth factor receptor and other growth factor ligand-receptor autocrine loops, increasing evidence suggests important roles for cytokines in mediating intracellular signaling events important in cell growth and survival. Interleukin-6 (IL-6) has been shown to activate pathways important in tumorigenesis including Janus kinase/signal transducer and activator of transcription, phosphotidylinositol 3-kinase/Akt, and extracellular signal-regulated kinase signaling. Using immunohistochemistry, we demonstrate that NSCLC specimens have tumor expression of IL-6 and IL-6 receptor components gp80 and gp130. These results suggest that IL-6 autocrine signaling might contribute to downstream signaling events in NSCLC and further support the concept of multiple autocrine pathways contributing to the pathogenesis of NSCLC.

Publication types

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

MeSH terms

  • Autocrine Communication*
  • Carcinoma, Non-Small-Cell Lung / metabolism*
  • Carcinoma, Non-Small-Cell Lung / pathology
  • Cytokine Receptor gp130 / metabolism*
  • Humans
  • Immunoenzyme Techniques
  • Interleukin-6 / metabolism*
  • Lung Neoplasms / metabolism*
  • Lung Neoplasms / pathology
  • Receptors, Interleukin-6 / metabolism*

Substances

  • Interleukin-6
  • Receptors, Interleukin-6
  • interleukin-6 receptor alpha
  • Cytokine Receptor gp130