Research Paper Volume 12, Issue 2 pp 1304—1321

AURKB promotes gastric cancer progression via activation of CCND1 expression

Figure 5. AZD1152 suppresses cell proliferation and represses the expression of CCND1 by inhibiting the enzymatic activity of AURKB in gastric cancer cells. (A) CCK-8 assays showing the effect of different concentrations of AZD1152 (0.5 μM, 2 μM and 10 μM; DMSO as the control) on the proliferation of SGC7901 and BGC823 cells. The results shown are the means ± SDs of three independent experiments; **, P < 0.01 compared with the DMSO control. (B) Colony formation assays showing the effects of different concentrations of AZD1152 (0.5 μM, 2 μM and 10 μM; DMSO as the control) on the colony formation ability of SGC7901 and BGC823 cells. Left panel, representative images from colony formation assays. Right panel, the number of colonies formed by the indicated cells was quantified. Data are presented as the means ± SDs; **, P<0.01 compared with the DMSO control. (C) Flow cytometry analysis showing the effect of different concentrations of AZD1152 (0.5 μM, 2 μM and 10 μM; DMSO as the control) on the cell cycle distribution. Bar graphs showing the percentages of SGC7901 and BGC823 cells in the G0/G1, S and G2/M phases when treated with different concentrations of AZD1152 (right panel). Each histogram bar represents the mean ± SD of three independent experiments. (D) Western blot analysis of the protein levels of AURKB, CCND1 and H3S10ph in SGC7901 and BGC823 cells treated with different concentrations of AZD1152 (0.5 μM, 2 μM and 10 μM; DMSO as the control). HSP70 and histone H3 were used as the endogenous loading controls. (E) Quantitative real-time PCR analysis of AURKB and CCND1 expression in SGC7901 and BGC823 cells treated with different concentrations of AZD1152 (0.5 μM, 2 μM and 10 μM; DMSO as the control); *, P < 0.05; **, P < 0.01. The results shown are the means ± SDs of three independent experiments. GAPDH was used as the endogenous control for mRNA expression analysis.