Objective: To explore the effect of corilagin on the proliferation

migration and invasion of human liver cancer cells and its relevant mechanism. Method: Methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay

transwell chamber and wound healing assay were used to evaluate the effect of corilagin on cell viability

cell cycle progression and migration of human liver cancer cells. Immunofluorescence staining and Western blot assays were performed to explore the effect on F-actin distribution

formation of lamellipodia and filopodia

and expressions of relevant signal molecules. Result: The MTT assay demonstrated that the proliferation of SMMC7721 and MHCC97H cell were inhibited by different concentrations of corilagin. Half maximal inhibitory concentrations (IC50) at 48 h were 388.67

314.42 μmol·L-1

respectively. Wound-healing assay showed that 200 μmol·L-1 corilagin exhibited the greatest inhibition on SMMC7721 cell

and 120 μmol·L-1 corilagin exhibited the greatest inhibition on MHCC97H cell. Transwell assay demonstrated that compared with negative control group

the number of penetrating cells in experimental group was decreased significantly. Immunofluorescence staining showed that corilagin can cause F-actin skeleton remodeling in SMCC7721 and MHCC97H cells. With higher concentrations

cell edge filopodia and lamellipodia formation gradually decreased

while fiber tension number increases gradually. This effect was significant in SMMC7721 200 μmol·L-1 and obvious in MHCC97H 120 μmol·L-1. Western blot showed that corilagin can significantly down-regulate protein expressions of N-Cad and Vimentin in EMT (P < 0.05)

and down-regulate MAPK pathway's p-ERK expression and increase p-p38 lightning protein expression (P < 0.05). Conclusion: Corilagin inhibited the proliferation

invasion and migration in human liver cancer cells in vitro. The mechanism may be correlated with the inhibition of N-Cad and Vimentin protein expressions and p-ERK expression

and up-regulation of p-p38 lightning protein expression.