FIGURE 2.

miR‐200c expression in parental CRC cells and colorectal CSCs. A, Relative basal expression of miR‐200c in LoVo cells (high metastatic potential) and HT29 cells (low metastatic potential), as well as isolated CSCs (LoVo‐CSCs and HT29‐CSCs), demonstrates a possible relationship between miR‐200c and metastatic property. B, miR‐200c expression in LoVo and HT29 cells relative to that of their corresponding CSCs. The same number of colorectal CSCs clearly exhibited higher miR‐200c expression than did CRC cells. C, miR‐200c expression was attenuated by ATL‐1 at 200 μM in both LoVo‐CSCs and HT29‐CSCs. D, Transfection efficiency of miR‐200c mimics (miR‐200c‐mim), inhibitors (miR‐200c‐inh), and their corresponding negative controls (miR‐200c‐mim‐NC and miR‐200c‐inh‐NC) in LoVo and HT29 cells. miR‐200c‐mim and miR‐200c‐inh, respectively, induced significant upregulation and downregulation of miR‐200c in LoVo and HT29 cells. E, The percentage of apoptotic LoVo and HT29 cells was increased by miR‐200c‐inh but remained unchanged in the case of miR‐200c‐mim. Relative proliferation of (F) LoVo and (G) HT29 cells subjected to transfection of miR‐200c mimics or inhibitors (or their corresponding NC). miR‐200c‐mim and miR‐200c‐inh, respectively, enhanced and inhibited the proliferation of both types of parental CRC cells. The data represent the mean ± SD of three independent technical replicates (t‐test or ANOVA); ^* P < .05; % P < .05 at 72 h