Glycolipid sulfotransferase activity in a human renal cell carcinoma cell line, SMKT-R3, is enhanced by epidermal growth factor (EGF); tyrosine kinase inhibitors suppress this enhancement. To investigate the involvement of Ras in the signal transduction pathway from the EGF receptor to the expression of glycolipid sulfotransferase, we introduced v-H-ras into SMKT-R3 cells. In a quiescent state, the percent GTP bound to Ras in v-H-ras-expressing cells increased about 2.5-fold compared with control cells, suggesting that v-Ras introduced into the renal cancer cells is in an active form without EGF stimulation. Glycolipid sulfotransferase activity in v-H-ras-expressing cells was higher than in control cells. The sulfotransferase activity was affected neither by EGF nor by genistein, a tyrosine kinase inhibitor, in v-H-ras-expressing cells, whereas it was enhanced by EGF and reduced by genistein in control cells. Our observations suggest that Ras mediates the regulation pathway of glycolipid sulfotransferase activity in SMKT-R3 cells.
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