Actein ameliorates hepatobiliary cancer through stemness and p53 signaling regulation

Area of Science:

• Pharmacology
• Hepatology
• Oncology

Background:

• Actein, a triterpene glycoside from Cimicifuga foetida, inhibits breast cancer cell proliferation.
• The role of actein in preventing liver injury and early liver cancer remains largely unknown.

Purpose of the Study:

• To investigate the therapeutic potential of actein in a mouse model of early liver cancer induced by diethylnitrosamine (DEN).

Main Methods:

• Liver cancer was induced in mice using DEN, followed by treatment with varying concentrations of actein.
• Histological analysis and assessment of proliferation and cancer stem cell markers (Cyclin Ds, p53, CD133) were performed.
• Expression levels of hypoxia-inducible factor-1α (Hif-1α) and vascular endothelial growth factor receptor 1 (VEGFR1) were evaluated.

Main Results:

• DEN-induced liver injury, characterized by steatohepatitis, fibrosis, and inflammation, was significantly ameliorated by actein treatment.
• Actein reversed DEN-induced hepatobiliary cysts and suppressed the expression of proliferation markers (Cyclin Ds, p53) and cancer stem cell markers (CD133).
• Actein administration reduced the upregulation of Hif-1α and VEGFR1 in DEN-treated liver tissues.

Conclusions:

• Actein demonstrates protective effects against DEN-induced liver injury and cancer progression in mice.
• Actein exhibits inhibitory effects on key molecular pathways involved in liver cancer development.
• Actein represents a promising therapeutic candidate for future liver cancer treatment strategies.