Fig. 4: SLC38A5 and CDH17 participate in drug resistance in colon cancer.

A Cell viability assays were performed on the indicated cell lines treated with different concentrations of 5-FU or CPT-11 for 48 h. B Apoptosis assays were conducted on the same cell lines treated with 5-FU (2 μM) or CPT-11 (20 μM) for 48 h. Analysis of SLC38A5 expression in LGR5-silenced cells by Western blot (C) and flow cytometry (D). SLC38A5 expression in the cell surface was significantly inhibited (*p < 0.05) following SLC38A5 or LGR5 silencing. E Western blot analysis of LGR5 and SLC38A5 in cell lines transfected with control or CDH17-targeting siRNAs and re-transfected after 48 h. Cell lysates were taken at 0, 48 and 96 h from the first transfection. Band quantification relative to control cells is shown. Cell viability (F) and apoptosis detection (G) assays were performed on KM12SM and SW620 cells previously transfected twice in 48 h with control or CDH17-targeting siRNAs and incubated for 48 h more in the presence of the indicated drugs. Stable or extended CDH17 silencing resulted in an increased percentage of apoptotic cells or a reduction in the percentage of viable cells following siRNA treatment (*p < 0.05;**p < 0.01;***p < 0.001). Data are representative of three independent experiments.