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[1]余越美,严巧灵,章康健,等.冬凌草甲素诱导乳腺癌Bcap37细胞凋亡的探索[J].浙江理工大学学报,2013,30(03):377-382.
　YU Yuemei,YAN Qiaoling,ZHANG Kangjian,et al.Exploration on Induction of Breast Cancer Bcap37 Apoptosis by Oridonin[J].Journal of Zhejiang Sci-Tech University,2013,30(03):377-382.
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冬凌草甲素诱导乳腺癌Bcap37细胞凋亡的探索()
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浙江理工大学学报[ISSN:1673-3851/CN:33-1338/TS]

卷:
第30卷
期数:
2013年03期
页码:
377-382
栏目:
(自科)生物与生命科学
出版日期:
2013-05-10

文章信息/Info

Title:
Exploration on Induction of Breast Cancer Bcap37 Apoptosis by Oridonin
文章编号:
1673-3851 (2013) 03-0377-06
作者:
余越美;  严巧灵;  章康健;  岳学田;  周秀梅
浙江理工大学生命科学学院新元医学与生物技术研究所, 杭州 310018
Author(s):
YU Yuemei;  YAN Qiaoling;  ZHANG Kangjian;  YUE Xuetian;  ZHOU Xiumei
Xinyuan Institute of Medicine and Biotechnology, School of Life Sciences, Zhejiang Sci-Tech University, Hangzhou 310018, China
关键词:
冬凌草甲素;  细胞凋亡;  乳腺癌;  Caspase;  survivin;  GADD34
分类号:
Q789
文献标志码:
A
摘要:
探讨冬凌草甲素(oridonin)对人乳腺癌细胞Bcap37的增殖、凋亡以及引起细胞凋亡机制。以不同浓度的Ori处理Bcap 37细胞,通过MTT法检测细胞生长抑制率;应用流式细胞分析术检测细胞凋亡; Western Blot检测细胞发生凋亡的机制。结果是48~96 μmol/L的Ori可显著抑制Bcap 37细胞的增殖(P <0.05)。48 μmol/L的Ori作用24 h后,细胞的增值抑制率达到了40%,而96 μmol/L的Ori只需处理12 h,增值抑制率竟达到了50%。 96 μmol/L Ori处理24 h后,Bcap 37细胞的凋亡率为21.6%。Western Blot检测到了Fas的上调,细胞色素c的释放和随后Caspase 9的激活及其下游信号蛋白Caspase 3和它的底物PARP,ICAD的剪切。进一步检测到Survivin的下调和GADD34的上调。基于这些实验结果,推测冬凌草甲素作为一种潜在的抗乳腺癌制剂,诱导乳腺癌细胞Bcap37发生凋亡的发生可能与Survivin和GADD34相关。

参考文献/References:

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备注/Memo

备注/Memo:
收稿日期： 2012-09-10
基金项目： 浙江理工大学科研启动基金(1116818 Y)
作者简介： 余越美(1982-),女,陕西咸阳人,硕士研究生,主要从事肿瘤的靶向基因病毒治疗的研究。
通信作者： 周秀梅,电子邮箱:zhouxiumei824@163.com
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