Skip to main content
. 2016 Dec 1;7(12):e2503. doi: 10.1038/cddis.2016.373

Figure 2.

Figure 2

Effect of miR-148a-3p on bladder cancer cell proliferation. (a) CCK-8 assay. The relative cell viability of the miR-148a-3p-treated groups of T24 and UM-UC-3 cells was lower than that of NC-treated groups (cell viability of 0 nM was regarded as 1.0). (b) Colony formation assay (representative wells are presented). The colony formation rate was lower for miR-148a-3p (50 nM)-transfected groups compared with NC (50 nM)-transfected groups. (c) Flow cytometric analysis (representative images are presented) of cell cycle distribution. miR-148a-3p overexpression induced a significant accumulation of cells in the G1-phase and blocked entry into G1-S. (d) Western blot analysis. miR-148-3p (50 nM) inhibited the cell cycle and the expression of AKT2 signaling-related proteins in T24 and UM-UC-3 cells. (eg) Tumor xenograft model. Tumor volumes and growth curves indicated that tumors in the miR-148a-3p group grew more slowly. Decreased Ki-67 expression and increased miR-148a-3p were also detected in miR-148a-3p-treated tumors. Error bars represent the S.E. obtained from three independent experiments; *P<0.05. Scale bar=100 μm