Riccardin D-26，一种合成的大环双苄基化合物，通过依赖 p53 的方式诱导细胞凋亡来抑制人肝癌细胞生长。
Riccardin D-26, a synthesized macrocyclic bisbibenzyl compound, inhibits human hepatocellular carcinoma growth through induction of apoptosis in p53-dependent way.
机构信息
Department of Pharmacology, Key Laboratory of Chemical Biology, School of Pharmaceutical Sciences, Shandong University, China.
出版信息
Cancer Lett. 2013 Jan 1;328(1):104-13. doi: 10.1016/j.canlet.2012.09.002. Epub 2012 Sep 18.
Riccardin D-26 is a synthesized macrocyclic bisbibenzyl compound. We investigated the effect of Riccardin D-26 on human hepatocellular carcinomas. Riccardin D-26 possessed stronger activity against SMMC-7721 cells than human normal liver cells. Riccardin D-26 injection effectively delayed the growth of SMMC-7721 xenografts in mice without significant toxicity. This effect of Riccardin D-26 was associated with the status of p53 and its targets, bax and p21(Waf1)(/)(Cip1). Riccardin D-26 activated p53 expression and induced cancer cells to apoptosis through the p53-mediated transcription-dependent and -independent pathway. Overall, Riccardin D-26 may inhibit hepatocellular carcinoma growth through induction of apoptosis in p53-dependent pathway.
瑞卡西林 D-26 是一种合成的大环双苄基化合物。我们研究了瑞卡西林 D-26 对人肝癌细胞的影响。瑞卡西林 D-26 对 SMMC-7721 细胞的活性强于正常人类肝细胞。瑞卡西林 D-26 注射剂在不产生显著毒性的情况下有效延缓了 SMMC-7721 异种移植瘤在小鼠体内的生长。瑞卡西林 D-26 的这种作用与 p53 及其靶标 bax 和 p21(Waf1)(/)(Cip1)的状态有关。瑞卡西林 D-26 通过 p53 介导的转录依赖性和非依赖性途径激活 p53 表达，并诱导癌细胞凋亡。总的来说，瑞卡西林 D-26 可能通过 p53 依赖性途径诱导细胞凋亡来抑制肝癌的生长。
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