Fig. 6

The effect of IVM on the EGFR signaling pathway. a-g The cell viability (a, b, and e), the protein expression levels of p-EGFR/EGFR and P-gp (c and f), and the mRNA level of MDR1 (d and g) of HCT-116 cells (WT) and EGFR knockout HCT-116 cells (EGFR-KO) treated with different concentrations of IVM or VCR (a), or treated with VCR in the presence of IVM (b, c) or LAP (e, f) or treated with IVM alone (d) or LAP alone (g) for 48 h were determined. The numbers in the figure keys in b and e represent the concentrations (μM) of IVM or LAP. h The cell viability of the VCR-resistant HCT-8 cells pretreated with IVM or VRP for 48 h, and then treated with VCR alone or VCR plus IVM, or VCR plus VRP for another 48 h were detected. Cell viability was determined by MTT assay and the protein expression levels were detected by Western blotting analysis using GAPDH as internal control. Cells treated with vehicle serve as control. Abbreviations: IVM, ivermectin; LAP, lapatinib; VCR, vincristine; VRP: verapamil; WT, HCT-116 cell; EGFR-KO, EGFR-knockout HCT-116 cells. Data in a, b, and e were conducted in quintuplicates and data were expressed as the mean ± SD (n = 5). Data in c and f are the representative of two independent experiments. Data in d and g are expressed as the mean ± SD (n = 3). Data in h represent the percentage of respective control values (mean ± SD, n = 5). Statistical significances in d, g, and h were determined using one-way ANOVA followed by Dunnett’s test. ^**P < 0.01, compared with the respective vehicle controls; ^#P < 0.05, ^##P < 0.01, comparison between the two columns; ns, no significance (P > 0.05), comparison between the two columns