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Controls of EGF‐induced morphological transformation of human bronchial epithelial cells
Author(s) -
Beckmann Joe D.,
Stewart Annette,
Kai Mark,
Keeton Timothy P.
Publication year - 2001
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.10013
Subject(s) - epidermal growth factor , tyrosine phosphorylation , phosphorylation , microbiology and biotechnology , transformation (genetics) , biology , epidermal growth factor receptor , growth factor , receptor , tyrosine kinase , cell culture , protein kinase c , endocrinology , signal transduction , chemistry , biochemistry , genetics , gene
Human bronchial epithelial cells, both normal primary (NHBE) and the BEAS‐2B line, respond to epidermal growth factor (EGF) by extruding lengthy filaments, or filapodia. The morphological transformation of BEAS‐2B cells maximized at 48 h using 1–10 nM EGF. EGF‐induced filapodia extension was inhibited by co‐exposure to transforming growth factor beta, which did not affect tyrosine phosphorylation of the EGF receptor (EGFR). Inhibition was also effected by phorbol myristoyl acetate (PMA), which reduced the rate of EGFR tyrosine phosphorylation. Dibutyryl‐cAMP had no effect, whereas the protein kinase inhibitor H‐89 stimulated the EGF response. The ability to regulate cellular responses to EGF by hormonal and chemical approaches has implications for current investigations into the roles of EGF in lung growth, differentiation, and wound repair. © 2001 Wiley‐Liss, Inc.