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Arsenic trioxide (As_2O_3) induced apoptosis and its mechanisms in a human esophageal squamous carcinoma cell line

机译:三氧化二砷(As_2O_3)诱导人食管鳞癌细胞凋亡及其机制

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Objective To study whether As_2O_3 has an apoptotic effect on human solid tumor cells, and the possible cellular and molecular mechanisms of this treatment using human esophageal squamous carcinoma cells (EC8712) as a model. Methods DNA microarray, biochemical and cytological analyses were used. Results The growth and survival of EC8712 cells were markedly inhibited by As_2O_3 treatment at a concentration of 1, 2 and 4 pmol/L. EC8712 cells were obviously arrested at G2/M phase with As2O3 treatment and apoptosis induced at micromolar As_2O_3 concentrations, as shown by morphology, histogram related nuclear DNA contents, and DNA gel electrophoresis. As_2O_3 activated caspase-3, which might be involved in the process of As_2O_3, induced apoptosis in EC8712 cells. Conclusions As_2O_3 changes the expression of many genes at transcription level. The regulation of expression of many genes might be involved in the process of As_2O_3 inducing apoptosis. These results suggest that As_2O_3 can be clinically useful for solid tumor treatment.
机译:目的以人食管鳞癌(EC8712)为模型研究As_2O_3是否对人实体瘤细胞具有凋亡作用,并探讨其可能的细胞和分子机制。方法采用DNA芯片,生化及细胞学分析。结果As_2O_3处理1、2和4 pmol / L能明显抑制EC8712细胞的生长和存活。如形态,直方图相关核DNA含量和DNA凝胶电泳所示,EC8712细胞在As2 / O3处理下明显被阻滞在G2 / M期,并在微摩尔As_2O_3浓度下诱导凋亡。 As_2O_3激活的caspase-3可能参与As_2O_3的过程,诱导EC8712细胞凋亡。结论As_2O_3在转录水平上改变了许多基因的表达。 As_2O_3诱导细胞凋亡的过程可能涉及许多基因的表达调控。这些结果表明,As_2O_3在临床上可用于实体瘤治疗。

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