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Am J Physiol Cell Physiol 281: C886-C898, 2001;
0363-6143/01 $5.00
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Vol. 281, Issue 3, C886-C898, September 2001

EGF receptor function is required in late G1 for cell cycle progression induced by bombesin and bradykinin

Chintda Santiskulvong, James Sinnett-Smith, and Enrique Rozengurt

Department of Medicine, School of Medicine and Molecular Biology Institute, University of California, Los Angeles, California 90095-1786

We examined the role of epidermal growth factor (EGF) receptor (EGFR) tyrosine kinase activation in G protein-coupled receptor (GPCR) agonist-induced mitogenesis in Swiss 3T3 and Rat-1 cells. Addition of EGFR tyrosine kinase inhibitors (e.g., tyrphostin AG-1478) abrogated bombesin-induced extracellular signal-regulated kinase (ERK) activation in Rat-1 cells but not in Swiss 3T3 cells, indicating the importance of cell context in determining the role of EGFR in ERK activation. In striking contrast, treatment with tyrphostin AG-1478 markedly (~70%) inhibited DNA synthesis induced by bombesin in both Swiss 3T3 and Rat-1 cells. Similar inhibition of bombesin-induced DNA synthesis in Swiss 3T3 cells was obtained using four structurally different inhibitors of EGFR tyrosine kinase. Furthermore, kinetic analysis indicates that EGFR function is necessary for bombesin-induced mitogenesis in mid-late G1 in both Swiss 3T3 and Rat-1 cells. Our results indicate that EGFR kinase activity is necessary in mid-late G1 for promoting the accumulation of cyclins D1 and E and implicate EGFR function in the coupling of GPCR signaling to the activation of the cell cycle.

epidermal growth factor receptor transactivation; tyrphostin AG-1478; G protein-coupled receptors; Swiss 3T3 cells; mitogen-activated protein kinases


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