Actein ameliorates hepatobiliary cancer through stemness and p53 signaling regulation.

Actein is isolated from the rthizomes of Cimicifuga foetida, which is a triterpene glycoside, displaying suppressive effects on breast cancer cells proliferation. However, the effects of actein treatment on liver injury, tending to cancer, have little to be known. Thus, the study is conducted to explore the role of actein in early liver cancer. Diethylnitrosamine (DEN) was used to induce liver cancer in mice followed by actein treatment at different concentrations. DEN caused steatohepatitis supported by fibrosis and inflammation, which were ameliorated for actein administration. Liver histology of mice with DEN treatment displayed hepatobiliary cysts, reversed by actein. Cell proliferation markers of Cyclin Ds and p53, as well as cancer stem cell markers of CD133 were highly increased in liver tissue samples from DEN-induced mice, and actein showed inhibitory role in these signals expression. Actein-reduced up-regulation of Hif-1α and VEGFR1 in DEN-stimulated liver tissue of mice was seen. Taken together, DEN promoted liver cancer progression, which was ameliorated by actein, supplying a potential therapeutic strategy for liver cancer in future.