Src Stimulates Insulin-like Growth Factor I (IGF-I)-dependent Cell Proliferation by Increasing IGF-I Receptor Number in Human Pancreatic Carcinoma Cells1

نویسندگان

  • Berenike B. M. Flossmann-Kast
  • Peter M. Jehle
  • Andreas Hoeflich
  • Guido Adler
  • Manfred P. Lutz
چکیده

We examined the potential function of Src in human pancreatic carci noma. Overexpression of kinase-activated SrcY527F resulted in a signif icant increase of insulin-like growth factor I (IGF-I)-dependent cell pro liferation in the cell line PANC-1. Western blotting and competition binding studies demonstrated 2.3 ±0.2-fold increase in IGF-I receptor expression and 2.8 ±0.4-fold increase in IGF-I-specific binding sites/cell. SrcY527F transfection alone did not change receptor affinity or basal receptor tyrosine phosphorylation, whereas IGF-I-stimulated receptor phosphorylation was increased by 2.1 ±0.5-fold. IGF-I m UN A expression and protein secretion did not change to exclude autocrine activation. We conclude that Src stimulates IGF-I-dependent proliferation of PANC-1 cells by increasing the number of IGF-I receptors/cell.

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Src stimulates insulin-like growth factor I (IGF-I)-dependent cell proliferation by increasing IGF-I receptor number in human pancreatic carcinoma cells.

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تاریخ انتشار 2006