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c‐Myc is required for transformation of FDC‐P1 cells by EGFRvIII
Author(s) -
Rath Oliver,
Himmler Adi,
Baum Anke,
Sommergruber Wolfgang,
Beug Hartmut,
Metz Thomas
Publication year - 2007
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2007.04.077
Subject(s) - tyrosine kinase , chemistry , receptor tyrosine kinase , cancer research , stimulation , function (biology) , tyrosine , transformation (genetics) , receptor , microbiology and biotechnology , tyrosine kinase inhibitor , biology , biochemistry , gene , endocrinology , cancer , genetics
In contrast to wtEGFR, its truncated version EGFRvIII transformed non‐tumorigenic FDC‐P1 cells only when c‐Myc was coexpressed. In nude mice, EGFRvIII/c‐Myc coexpressing cells induced tumors, whereas wtEGFR‐expressing EGF‐dependent FDC‐P1 cells did not. EGFRvIII function was required for both the induction and maintenance of tumor growth. Cellular proliferation was inhibited by a selective EGFR tyrosine kinase inhibitor indicating intrinsic tyrosine kinase activities for both receptors. Unlike wtEGFR, constitutive signaling by EGFRvIII was refractory to stimulation by the EGFR ligands EGF and TGF‐α. Summarized, EGFRvIII is a constitutively active receptor tyrosine kinase whose transforming capacity is lower than that of EGF‐stimulated wtEGFR.