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DICO,一种新型非芳香族 B 环黄酮类化合物,可诱导人肝癌细胞 G2/M 期细胞周期阻滞和凋亡。

DICO, a novel nonaromatic B-ring flavonoid, induces G2/M cell cycle arrest and apoptosis in human hepatoma cells.

机构信息

Beijing Institute of Biotechnology, Beijing 100000, China.

出版信息

Food Chem Toxicol. 2013 Jul;57:322-9. doi: 10.1016/j.fct.2013.03.032. Epub 2013 Apr 6.

DOI:10.1016/j.fct.2013.03.032
PMID:23567243
Abstract

DICO was a novel nonaromatic B-ring flavonoid obtained from Macrothelypteris torresiana. In the present work, we investigated the antitumor activity and the antineoplastic mechanism of DICO. Our study showed that DICO inhibited the growth of HepG2 cells in dose and time-dependent manners. As well as DICO induced G2/M cell cycle arrest and apoptosis via a ROS-mediated mitochondrial pathway. Western blot assay demonstrated that DICO decreased Bcl-2 level and induced Bax translocation to cause cytochrome c release. Subsequently, caspase-9 and caspase-3 were activated. Meanwhile, the alterations of cyclin A and B1, p-CDK1 and p-cdc25c levels were also observed in response to DICO treatment. Taken together, DICO displayed a significant antitumor effect through G2/M cell cycle arrest and apoptosis induction, which suggested DICO might have therapeutic potential against tumors.

摘要

DICO 是一种新型非芳香族 B 环类黄酮,从中国蕨Macrothelypteris torresiana 中提取得到。在本工作中,我们研究了 DICO 的抗肿瘤活性和抗肿瘤机制。我们的研究表明,DICO 以剂量和时间依赖的方式抑制 HepG2 细胞的生长。此外,DICO 通过 ROS 介导的线粒体途径诱导 G2/M 细胞周期阻滞和细胞凋亡。Western blot 分析表明,DICO 降低了 Bcl-2 水平,并诱导 Bax 易位导致细胞色素 c 释放。随后,caspase-9 和 caspase-3 被激活。同时,还观察到 cyclin A 和 B1、p-CDK1 和 p-cdc25c 水平的改变,这也是对 DICO 处理的响应。总之,DICO 通过 G2/M 细胞周期阻滞和凋亡诱导显示出显著的抗肿瘤作用,这表明 DICO 可能具有治疗肿瘤的潜力。

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