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. 2017 Feb 19;50(3):e12341. doi: 10.1111/cpr.12341

Figure 2.

Figure 2

The ectopic expression of miR‐506 inhibited the proliferation of oxaliplatin‐resistant colorectal cancer cells. A, The cell viability of HCT116 and HCT116‐OxR were treated with different concentrations of oxaliplatin for 48 h. B, miR‐506 was down‐regulated in HCT116‐OxR cells. C, miR‐506 was up‐regulated in HCT116‐OxR cells via the transfection of a miR‐506 mimic. After 48 h, the level of miR‐506 was detected via qRT‐PCR. D, Overexpression of miR‐506 significantly decreased the growth‐inhibitory effect of oxaliplatin in HCT116‐OxR cells, as measured by MTT assay. E, The effect of miR‐506 on the cell cycle distribution of HCT116‐OxR was monitored via flow cytometry at 5 μg/mL oxaliplatin concentration. The miR‐506‐overexpression HCT116‐OxR cells were arrested at G1 phase of the cell cycle, resulting in a corresponding reducing in the percentage of cells in S and G2/M phases. F, The proportion of annexin V‐positive apoptotic cells was evaluated by flow cytometry using annexin V allophycocyanin and propidium iodide staining of HCT116‐OxR after transfection of a miR‐506 mimic. HCT116‐OxR cells were used as blank group and HCT116‐OxR‐miR‐Ctrl cells were used as negative control. The data are shown as the means ± SD of three replicates (*P<.05)