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Clin Lung Cancer. 2006 Jan;7(4):273-5.

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

Author information

1
Thoracic Oncology Program, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA. hauraeb@moffitt.usf.edu

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.

PMID:
16512982
DOI:
10.3816/CLC.2006.n.006
[Indexed for MEDLINE]

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