Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2049946 | FEBS Letters | 2007 | 8 Pages |
Abstract
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.
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Authors
Oliver Rath, Adi Himmler, Anke Baum, Wolfgang Sommergruber, Hartmut Beug, Thomas Metz,