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Journal of Biochemical and Molecular Toxicology 2017-Sep

Triggering p53 activation is essential in ziyuglycoside I-induced human retinoblastoma WERI-Rb-1 cell apoptosis.

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Krækjan er vistuð á klemmuspjaldið
Xue Zhu
Ke Wang
Yong Yao
Kai Zhang
Fanfan Zhou
Ling Zhu

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Útdráttur

Ziyuglycoside I (Ziyu I), one of the major components isolated from the root of Sanguisorba officinalis L., has been proved for the antitumor properties on oral cancer, prostate cancer, and colorectal cancer. However, the effect of Ziyu I on retinoblastoma (RB) is not well understood. In this study, we investigated the inhibitory effect and underlying molecular mechanism of Ziyu I on human RB WERI-Rb-1 cells. Our results indicated that Ziyu I could suppress cell viability and induce mitochondrial-dependent cell apoptosis in WERI-Rb-1 cells. Furthermore, Ziyu I treatment increased p53 expression as well as improved p53 stabilization through downregulation of pS166-Mdm2 and upregulation of phosphorylated- and acetylated-p53. Blockade of p53 significantly attenuated Ziyu I-induced mitochondrial dysfunction. Our findings demonstrate that Ziyu I exhibits excellent anticancer effect on human RB WERI-Rb-1 cells by triggering p53 activation, and imply Ziyu I as a potential compound for chemotherapy of human RB.

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