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Figure 2 | Breast Cancer Research

Figure 2

From: Penta-O-galloyl-β-D-glucose induces G1arrest and DNA replicative S-phase arrest independently of P21 cyclin-dependent kinase inhibitor 1A, P27 cyclin-dependent kinase inhibitor 1B and P53 in human breast cancer cells and is orally active against triple-negative xenograft growth

Figure 2

The effect of PGG on cell cycle distribution of MCF-7 (a) and MDA-MB231 (b) cells detected by propidium iodide/BrdU-bivariate flow cytometric analyses. Cells were exposed to increasing concentrations of PGG for 6, 24, and 48 hours. BrdU was added for the last 30 minutes to label S-phase cells active in DNA replication. Values are mean ± standard error of the mean (n = 4). Results are from two independent experiments with duplicate values at each concentration. The medium was not changed for PGG exposure of longer than 24 hours. Statistical significance: (a) BrdU incorporation at all three time points, one-way analysis of variance (ANOVA) P < 0.0001, with Dunnett's multiple comparison post test P value of less than 0.01 for 0 versus 12.5, 25, and 50 μM PGG. For G1, 6 hours P < 0.05 for 0 versus 25 and 50 μM PGG; 24 hours P < 0.01 for 0 versus 12.5 or 50 μM PGG; 48 hours P < 0.01 for 0 versus 12.5 μM PGG and P < 0.05 for 0 versus 50 μM PGG. For S, 24 hours/48 hours P < 0.01 for 0 versus 12.5 and 25 μM PGG. (b) BrdU incorporation at all three time points, one-way ANOVA P < 0.0001, with Dunnett's multiple comparison post test P value <0.01 for 0 versus 12.5, 25, and 50 μM PGG. For G1, 6 hours P < 0.05 for 0 versus 12.5, 25, and 50 μM PGG; 24 hours P < 0.01 for 0 versus 25 and 50 μM PGG; 48 hours P < 0.01 for 0 versus 50 μM PGG. For S, 24 hours/48 hours P < 0.01 for 0 versus 12.5 μM PGG. BrdU, 5-bromo-2'-deoxy-uridine; PGG, penta-O-galloyl-β-D-glucose.

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