OBJECTIVE: To investigate the effects of solasonine on the proliferative activity of hepatoma cells and the regulation of mitogen-activated protein kinase/extracellular signaling regulation kinase（MAPK/ERK） signaling pathway. METHODS: HepG2 cells in logarithmic growth phase were randomly divided into the control group

solasonine group（cells treated with 50 μmol/L solasonine）

activator group（cells treated with 20 μmol/L ISO） and activator + solasonine group（cells treated with 50 μmol/L solasonine after 24 h of treatment with 20 μmol/L ISO）. After 24 h

MTT assay was used to detect cell viability

scratch assay was used to detect cell migration

transwell assay was used to detect cell invasion

and Western blotting was used to detect the relative expression levels of p-ERK

ERK

mitogen activated protein kinase kinase（MEK） and p-MEK protein. RESULTS: Compared with the 0 μmol/L solasonine group

the cell viability of 10

20

30

40 and 50 μmol/L solasonine group decreased significantly（P<0.05）

the difference was concentration-dependent. Compared with the control group

the cell survival rate

scratch healing rate and relative expression levels of p-ERK and p-MEk protein and number of invasive cells in the solasonine group decreased

while the scratch healing rate and relative expression levels of p-ERK and p-MEk protein and number of invasive cells in the activator group increased

with statistically significant differences（P<0.05）. Compared with the solasonine group

the cell survival rate

scratch healing rate and relative expression levels of p-ERK and p-MEk protein and number of invasive cells increased in activator + solasonine group

with statistically significant difference（P<0.05）. Compared with the activator group

the cell survival rate

scratch healing rate and relative expression levels of p-ERK and p-MEk protein and number of invasive cells decreased in the activator + solasonine group

with statistically significant difference（P<0.05）. CONCLUSIONS: Solasonine can reduce the proliferation

migration and invasion of hepatocellular carcinoma cells

possibly by inhibiting MAPK/ERK signaling pathway.