Skip to main content
Figure 3 | Molecular Cancer

Figure 3

From: Colon cancer-derived oncogenic EGFR G724S mutant identified by whole genome sequence analysis is dependent on asymmetric dimerization and sensitive to cetuximab

Figure 3

Dimerization disruption has effects on the transforming activity of G719S and G724S EGFR proteins. (A and B) G719S and G724S mutants are dependent on asymmetric dimerization for their transforming potential. NIH-3T3 cells expressing the indicated EGFR mutants with or without receiver-impairing (L704N) or/and activator-impairing (I941R) mutations were assayed for anchorage-independent growth in soft agar. The bar graph depicts the relative number of colonies in the dimerization-defective mutants normalized to the number of colonies formed by cells expressing the respective parental mutants (n = 3, mean + SD). (C and D) Ligand-induced and constitutive tyrosine-phosphorylation is abrogated on dimerization-impaired compound mutants of cetuximab-sensitive EGFR mutants. Whole cell lysates from the same cells analyzed in Figure 3A and B expressing G719S (C), and G724S (D) mutants with or/and without dimerization-impairing mutations (L704N or I941R) in the absence or presence of EGF treatment for 15 minutes (25 ng/ml) were subjected to immunoblotting with antibodies against phospho-tyrosine (4G10) and EGFR.

Back to article page