Controls of EGF-induced morphological transformation of human bronchial epithelial cells

Human bronchial epithelial cells, both normal primary (NHBE) and the BEAS-2 B line, respond to epidermal growth factor (EGF) by extruding lengthy filam ents, or filapodia. The morphological transformation of BEAS-2B cells maxim ized at 48 h using 1-10 nM EGF. EGF-induced filapodia extension was inhibit ed by coexposure to transforming growth factor beta, which did not affect t yrosine phosphorylation of the EGF receptor (ECFR). Inhibition was also eff ected by phorbol myristoyl acetate (PMA), which reduced the rate of EGFR ty rosine phosphorylation. Dibutyryl-cAMP had no effect, whereas the protein k inase inhibitor H-89 stimulated the EGF response. The ability to regulate c ellular responses to EGF by hormonal and chemical approaches has implicatio ns for current investigations into the roles of EGF in lung growth, differe ntiation, and wound repair. (C) 2001 Wiley-Liss, Inc.