A Hopeful Natural Product, Pristimerin, Induces Apoptosis, Cell Cycle Arrest, and Autophagy in Esophageal Cancer Cells

Figure 2

Eca109 and Ec9706 cells were exposed to various concentrations of pristimerin (0, 1.0, 1.5, and 4.0 μmol·L^–1) for 48 hours followed by the cell cycle distribution assay and altered CDK2, CDK4, cyclin E, and CDKN1B. The percentage of cells in G0/G1, S, and G2/M phases of the cell cycle following pristimerin treatment in Eca109 and Ec9706 cells (a, b). Western blotting was used to detect the ratios of CDK2, CDK4, cyclin E, and CDKN1B expression in Eca109 (c) and Ec9706 (d) cells treated with pristimerin (1.5 μmol·L^–1, 48 hours). Relative expression of CDK2, CDK4, cyclin E, and CDKN1B was normalized to β-actin. Data are the average of three independent experiments for each group. Comparable results were observed from another three experiments. versus control group.

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