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To study the effects of epidermal growth factor (EGF) on invasion and metastasis of human oral squamous cell carcinoma, we examined the intracellular signal transduction of EGF-induced motility using an EGF sensitive s-1 clone cell line, obtained from Ca9-22 cell line. EGF (1, 10, 100 ng/ml )treated s-1 cells were affected by some blocking chemicals, and modulation of random motility was examined by phagokinetic track assay. When the cells ware treated with erbstatin analog; to inhibit tyrosine phosphorylation, or psi-tectorigenin to inhibit phosphatidyl-inositol turnover the motility enhanced by EGF was completely inhibited. When phorbol 12-myristate 13-acetate (PMA) was used,to stimulate protein kinase C (PKC), motility in the absence of EGF was enhanced similar to that of EGF stimulation. Calphostin C, an inhibitor of PKC activation, completely eliminated the EGF-induced enhancement of motility. Examination of the intracellular localization of PKC with a confocal laser microscope showed enhanced expression of PKC and translocation of PKC to membrane area after EGF stimulation. These results suggest that activation of phospholipase C y (PLC y) caused by auto-phosphorylation of EGF receptor might play an important role in the signal transduction of EGF-induced motility.

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Inhibition of enhanced motility stimulated by EGF in subclone (s-1) cells of human oral squamous cell carcinoma cell line (Ca9-22). Effects of inhibition of intracellular signal transduction on cell motility.