首页> 外文期刊>Cancer letters >Riccardin D-26, a synthesized macrocyclic bisbibenzyl compound, inhibits human hepatocellular carcinoma growth through induction of apoptosis in p53-dependent way
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Riccardin D-26, a synthesized macrocyclic bisbibenzyl compound, inhibits human hepatocellular carcinoma growth through induction of apoptosis in p53-dependent way

机译:Riccardin D-26,一种合成的大环双联苄基化合物,通过以p53依赖性方式诱导细胞凋亡来抑制人肝癌的生长

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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 p21Waf1/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.
机译:瑞卡丁D-26是合成的大环双联苄基化合物。我们调查了Riccardin D-26对人肝细胞癌的影响。 Riccardin D-26对SMMC-7721细胞的活性比人正常肝细胞强。瑞卡丹D-26注射有效地延迟了SMMC-7721异种移植物在小鼠体内的生长,而没有明显的毒性。 Riccardin D-26的这种作用与p53及其靶标bax和p21Waf1 / Cip1的状态有关。 Riccardin D-26激活p53表达,并通过p53介导的转录依赖性和非依赖性途径诱导癌细胞凋亡。总体而言,Riccardin D-26可能通过诱导p53依赖性途径的凋亡来抑制肝癌的生长。

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