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Figure 2 | Molecular Cancer

Figure 2

From: Overcoming acquired resistance to cetuximab by dual targeting HER family receptors with antibody-based therapy

Figure 2

CtxRclones depend on EGFR and HER3 for proliferation and cetuximab response. (A) Effects of EGFR and HER3 knockdown on proliferation of CtxR cells. Proliferation was measured at 72 h after treatment using the crystal violet assay. Data points are represented as mean ± s.e.m (n = 3). *p ≤0.05. Whole cell lysates were harvested after 72 h treatment and fractionated on SDS-PAGE followed by immunoblotting for the indicated proteins. α-Tubulin was used as a loading control. (B) Upregulation of NRG-1 ligand in CtxR clones by real-time qPCR. NRG-1 expression level in CtxR clones HC1, HC4 and HC8 was measured by real-time qPCR analysis. Data are represented as fold increase relative to the HP parental control. Data points are represented as mean ± s.e.m. (n = 4). (C) NRG-1 ligands can enhance cetuximab resistance in cetuximab-sensitive cells. Proliferation was measured at 72 h after treatment using CCK8 assays and plotted as a percentage of proliferation relative to the vehicle cells. Data points are represented as mean ± s.e.m. (n = 4). (D) NRG-1 increased phosphorylation levels of HER family receptors and their respective kinase targets in HP cells. Whole cell lysates were harvested and fractionated on SDS-PAGE followed by immunoblotting for the indicated proteins. α-Tubulin was used as a loading control.

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