INTERFERON GAMMA-INDUCED EGF RECEPTOR TRANSACTIVATION DEPENDS ON IFNγ RECEPTOR EXPRESSION LEVEL IN EPITHELIAL
CELLS
I. V. Gonchar, V. N. Dorosh, N. N. Nikolsky, E. B. Burova 1
Institute of Cytology, RAS, St. Petersburg;
1 e-mail: lenbur87@mail.ru
Earlier, we demonstrated transactivation of the epidermal growth factor receptor (EGFR) in response to interferon gamma (IFNγ) in epidermal
carcinoma A431 cells. It was shown that IFNγ-induced EGFR transactiva-tion is impossible in some cancer epithelial cells. Here, we hypothesize that
IFNγ-dependent EGFR transactivation in these cells correlates with EGFR quantity on the cell surface. To test this suggestion, a line of stably transfected
HEK293 cells (HEK293Δ99 cells) expressing high level of mutant EGFR lacking 99 C-terminal residues has been established. HEK293Δ99 cells
demonstrated EGFR transactivation in response to IFNγ unlike the parent HEK293 cells, in which transactivation lacked. In HEK293Δ99 and A431 cells,
the time courses of EGFR activation induced by IFNγ have the same pattern. In HEK293Δ99 cells like A431, IFNγ-induced EGFR transactivation
requires EGFR kinase activity and occurs via autophosphorylation mechanism. Taken together, these data provide direct evidence of the dependence of
IFNγ-induced EGFR transactivation upon EGFR expression level in epithelial cells.
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