Intestinal metabolite compound K of panaxoside inhibits the growth of gastric carcinoma by augmenting apoptosis via Bid-mediated mitochondrial pathway.
Intestinal metabolite compound K of panaxoside inhibits the growth of gastric carcinoma by augmenting apoptosis via Bid-mediated mitochondrial pathway.
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人参皂苷的肠道代谢化合物 K 通过 Bid 介导的线粒体途径增强细胞凋亡来抑制胃癌的生长
DOI：
10.1111/j.1582-4934.2011.01278.x
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发表时间：
2012-01
影响因子：
5.3
通讯作者：
Hu T
中科院分区：
文献类型：
--
作者：
Hu C;Song G;Zhang B;Liu Z;Chen R;Zhang H;Hu T
化合物K（20-O-β-D-吡喃葡萄糖基-20（S）-原人参二醇，CK）是人参皂苷的肠道细菌代谢物，已显示出在多种肿瘤中抑制肿瘤生长。然而，所涉及的机制在很大程度上是未知的。本研究以人胃癌细胞系BGC 823、SGC 7901和人胃癌裸鼠移植瘤为模型，探讨CK在胃癌中的作用机制。结果发现，CK对胃癌细胞株BGC 823和SGC 7901的生长有明显的抑制作用，且呈剂量和时间依赖性。CK诱导BGC 823和SGC 7901细胞凋亡，细胞周期阻滞于G2期，其机制与p21蛋白表达上调，cdc 2和cyclin B1蛋白表达下调有关。进一步的研究表明，CK主要通过胞内途径诱导BGC 823和SGC 7901细胞凋亡，并诱导细胞核Bid向线粒体转位。CK对胃癌细胞株SGC 7901裸鼠成瘤有明显的抑制作用。我们的研究表明，CK可通过Bid介导的线粒体途径抑制人胃癌细胞的活力并诱导其凋亡。
Compound K (20-O-β-D-glucopyranosyl-20(S)-protopanaxadiol, CK), an intestinal bacterial metabolite of panaxoside, has been shown to inhibit tumour growth in a variety of tumours. However, the mechanisms involved are largely unknown. We use human gastric carcinoma cell lines BGC823, SGC7901 and human gastric carcinoma xenograft in nude mice as models to study the mechanisms of CK in gastric cancers. We found that CK significantly inhibits the viabilities of BGC823 and SGC7901 cells in dose- and time-dependent manners. CK-induced BGC823 and SGC7901 cells apoptosis and cell cycle arrest in G2 phase by up-regulation of p21 and down-regulation of cdc2 and cyclin B1. Further studies show that CK induces apoptosis in BGC823 and SGC7901 cells mainly through mitochondria-mediated internal pathway, and that CK induces the translocation of nuclear Bid to mitochondria. Finally, we found that CK effectively inhibited the tumour formation of SGC7901 cells in nude mice. Our studies show that CK can inhibit the viabilities and induce apoptosis of human gastric carcinoma cells via Bid-mediated mitochondrial pathway.
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影响因子：
4.8
作者：
Breitschopf, K;Zeiher, AM;Dimmeler, S
通讯作者：
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影响因子：
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