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. 2017 Jan 31;8(26):42043–42060. doi: 10.18632/oncotarget.14927

Figure 2. Effects of miR-1 on the growth of gastric and breast cancer cells and normal cells.

Figure 2

A. miR-1 overexpression in gastric cancer and normal cells. MGC-803, HGC-27, MKN45 and GES-1 cells were transfected with the miR-1 precursor or the negative control miRNA. At 48 h after transfection, the miR-1 expression was detected with quantitative real-time PCR. B. Cell proliferation rate. Cells were transfected with the precursor miR-1 or the negative control miRNA. From 1 d to 5 d after transfection, cell growth was examined using cell proliferation assays. C. Effects of miR-1 on the cell cycle. At 48 h after cells were transfected with the miR-1 precursor or the negative control, the cell cycle of cancer and normal cells was evaluated with flow cytometry. D. Cell senescence analysis. Cells transfected with the precursor miR-1 or the negative control miRNA were treated using senescence-associated β-galactosidase staining. Representative images are shown. Scale bar, 100 μm. E. Detection of pRb phosphorylation. Cells treated with the precursor miR-1 or the negative control miRNA were subjected to Western blot analysis with the phosphorylated pRb antibody (P-pRb). β-Actin was used as a control. F. Detection of gastric cancer cell apoptosis using flow cytometry. Cells transfected with the precursor miR-1 or the negative control miRNA were subjected to apoptosis assays with AnnexinV. G. The overexpression of miR-1 in breast cancer cells. Breast cancer cells (MDA-MB-231 and MDA-MB-435) were transfected with 30 nM of the miR-1 precursor or the negative control miRNA. After 48 h after, the cells were analyzed using quantitative real-time RT-PCR. H. The effect of miR-1 overexpression on breast cancer cell proliferation. Breast cancer cells were transfected with 30 nM of the miR-1 precursor or the negative control miRNA. Then, cell growth was examined daily. I. Effects of miR-1 overexpression on breast cancer cell cycle. The breast cancer cells transfected with the miR-1 precursor were subjected to cell cycle assays. In all panels, data are shown as mean ± standard deviation from three independent experiments (* p < 0.05; ** p < 0.01).