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. Author manuscript; available in PMC: 2010 Jul 13.
Published in final edited form as: Oncogene. 2008 Feb 25;27(28):3944–3956. doi: 10.1038/onc.2008.19

Figure 2. EGFR is upregulated in cetuximab-resistant cells.

Figure 2

A: Characterization of expression of HER family members and down stream Akt and MAPK in cetuximab-resistant clones (HC1, HC4-HC8). Protein was collected and fractionated by SDS-PAGE followed by immunoblotting for the indicated proteins. α-tubulin was used as loading control. HP; cetuximab-sensitive parental line, HC; cetuximab-resistant clones.

B: EGFR has increased association with HER2, HER3, and cMET in cetuximab-resistant cells. Cetuximab-resistant cells were harvested and EGFR was immunoprecipitated from the cetuximab-resistant clone HC4 and the parental HP cells with an anti-EGFR antibody. The immunoprecipitates were fractionated on SDS-PAGE followed by immunoblotting for the indicated proteins. HP; cetuximab-sensitive parental line, HC4; cetuximab-resistant clone.

C: Cetuximab treatment does not modulate EGFR phosphorylation in cetuximab-resistant clone (HC4). Parental cells (HP) and cetuximab-resistant clone (HC4) were treated with vehicle (control) or increasing concentrations of cetuximab (CTX) for 24 hours. Stimulation was with EGF (10ng/ml) and HRG (5μM) for 45 minutes. Protein was collected and fractionated by SDS-PAGE followed by immunoblotting for the indicated proteins. α-tubulin was used as a loading control.