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Departments of Internal Medicine I [B. B. M. F., G. A., M. P. L.] and Internal Medicine II [P. M. J.] University of Ulm, 89070 Ulm, Germany, and Institute of Molecular Animal Breeding, University of Munich, 81377 Munich, Germany [A. H.]
We examined the potential function of Src in human pancreatic carcinoma. Overexpression of kinase-activated SrcY527F resulted in a significant increase of insulin-like growth factor I (IGF-I)-dependent cell proliferation 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 mRNA 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.
1 This work was supported by the Deutsche Forschungsgemeinschaft (Lu 441/2-2) and by the Bundesministerium für Bildung, Wissenschaft, Forschung und Technik, together with the Land Baden-Württemberg (01 KS 9609/2 and Landesforschungsschwerpunkt II-7532.22-19/23).
2 To whom requests for reprints should be addressed, at Department of Internal Medicine I, University of Ulm, Robert-Koch-Str. 8, 89070 Ulm, Germany. Phone: 49 731 502 4319; Fax: 49 731 502 4323; E-mail: manfred.lutz@medizin.uni-ulm.de.
Received 5/15/98. Accepted 7/ 1/98.
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