| 叶福林 冯英备 张玉景 尹苏芹 周峰 冯英同.水飞蓟宾通过抑制Notch1 信号通路发挥抗食管癌EC109 细胞的作用[J].,2015,15(24):4620-4623 |
| 水飞蓟宾通过抑制Notch1 信号通路发挥抗食管癌EC109 细胞的作用 |
| Silybin Exerts Antitumor Activity in Human Esophageal Cancer EC109 CellLine by Inhibiting Notch1 Signaling Pathway |
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| DOI： |
| 中文关键词: 水飞蓟宾 食管癌 EC109 细胞系 凋亡 Notch1 信号通路 |
| 英文关键词: Silybin Esophageal cancer EC109 cell line Apoptosis Notch1 signaling pathway |
| 基金项目:国家自然科学基金项目（81201583） |
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| 摘要点击次数: 855 |
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| 中文摘要: |
| 目的：探讨水飞蓟宾(silybin，SIL)对人食管癌EC109细胞系的作用，并探求Notch1 以及凋亡通路在其中的角色。方法：实验
分为对照组和SIL处理组(75、150、300 uM)，各组细胞分别处理12、24、36 小时。Cell Counting Kit-8 (CCK-8) 测细胞活力；粘附实
验测细胞粘附能力；Caspase-Glo誖3/7 定量试剂盒测细胞Caspase3/7 的表达；Western-blot 测Notch1、Bcl2 和Bax 蛋白表达。结
果：CCK-8 检测结果示SIL 可有效抑制EC109 细胞的活力(P<0.01)，并呈浓度时间依赖性；粘附实验结果示SIL可以降低EC109
细胞粘附能力(P<0.01)；Caspase3/7检测结果示SIL可以使EC109 细胞Caspase3/7 活性升高(P<0.01)；Western-blot 检测结果显示
SIL可以使EC109 细胞Notch1 和Bcl2 表达下降，Bax 表达上升(P<0.01)。结论：SIL可有效抑制食管癌EC109 细胞活力，其作用
机制可能与抑制Notch1 通路，激活凋亡通路相关，SIL可能是食管癌药物治疗领域具有开发前景的药物 |
| 英文摘要: |
| Objective:To investigate the effects of silybin (SIL) on esophageal cancer EC109 cell line and the roles of notch1 and
apoptosis pathway in it.Methods:The cells were divided into the control group and SILgroups (75, 150, 300 uM), each group was treated
for 12, 24 and 36 h. Cell Counting Kit-8 (CCK-8) was used to measure the cell viability; adhesion assay was used to determinate the adhesive
rate of cells; Caspase-Glo誖3/7 assay kit was used to detect the activity of Caspase 3/7; Western-blot was used to detect the expression
of Notch1, Bcl2 and Bax proteins.Results:The CCK-8 results showed that SIL could inhibit the cell viability of EC109 cells in a
dose and time-dependent manner (P<0.01). The results of adhesion experiment showed that SIL could weaken the adhesive capacity of
EC109 cells in a dose-dependent manner (P<0.01). After being treated with SIL, the activity of Caspase3/7 was increased significantly
(P<0.01). In addition, Western-bolt results showed that SIL treatment not only decreased the expression of Notch1 and Bcl2 proteins, but
also increased the expression of Bax protein in EC109 cells (P<0.01).Conclusion:SIL treatment can effectively inhibit the viability of
EC109 cells, the mechanisms of which may be related to the inhibition of notch1 and activation of apoptosis pathway, and SIL may be a
potential new drug in treatment of esophageal cancer. |
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