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Aim: To study the anticancer activity of sodium caffeate (SC). Methods: A nucleoside transport assay was used to analyze the inhibitory effects of SC on nucleoside rescue. The MTT assay was used to measure cell proliferation. Flow cytometrywas used to measure the apoptosis of BEC-7402 induced by SC and the cell cycledistribution change. Western blotting analysis was employed to investigate Bcl2, caspase and Bax expression. Intracellular Ca~(2+) and mitochondrial membranepotential were determined by flow cytometry. In vivo anti-tumor activity wasmeasured using a tumor transplantation model in mice. Results: SC inhibited thenucleoside transport of BEL-7402 cells with an IC_(50) of 1.02 mg/mL. SC inhibitedtumor cell proliferation with an IC_(50) between 100 μg/mL and 200μg/mL. SC induced BEL-7402 cell apoptosis in a time-and dose-dependent manner, which wasinduced by arresting cells in S phase. The in vivo study showed that tumorgrowth was inhibited in a dose-dependent manner. Activated caspase-3 and Baxexpression were up-regulated after treatment with SC, while Bcl-2 expression wasdown-regulated. Intracellular Ca~(2+) was increased while mitochondrial membranepotential was decreased by SC. Conclusion: SC is a new anticancer agent withpromising potential.
Aim: To study the anticancer activity of sodium caffeate (SC). Methods: A nucleoside transport assay was used to analyze the inhibitory effects of SC on nucleoside rescue. The MTT assay was used to measure cell proliferation. of BEC-7402 induced by SC and the cell cycled distribution change. Western blotting analysis was employed to investigate Bcl2, caspase and Bax expression. Intracellular Ca ~ (2+) and mitochondrial membrane potential were determined by flow cytometry. In vivo anti-tumor activity wasmeasured Results: SC inhibited thenucleoside transport of BEL-7402 cells with an IC 50 of 1.02 mg / mL. SC inhibited tumor cell proliferation with an IC 50 between 100 μg / mL and 200 μg / mL . SC induced BEL-7402 cell apoptosis in a time-and dose-dependent manner, which was induced by arresting cells in S phase. The in vivo study showed that tumorgrowth was inhibited in a dose- dependent manner. Activated The expression of caspase-3 and Baxexpression were up-regulated after treatment with SC, while Bcl-2 expression wasdown-regulated. Intracellular Ca ~ (2+) was increased while mitochondrial membrane potential was decreased by SC. Conclusion: SC is a new anticancer agent withpromising potential .