ABSTRACT
OBJECTIVE@#To investigate the relationship between the anti-proliferation effect of baicalein and extracellular signal-regulated kinase and focal adhesion kinase(ERK-FAK) signal pathway in oral squamous cell carcinoma (OSCC).@*METHODS@#The study included two parts and each part contained 4 groups, including control, 20 μmol/L BAI, 40 μmol/L BAI, 80 μmol/L BAI or control, 40 μmol/L BAI, MEK inhibitor(0.33 nmol/L),MEK inhibitor(0.33 nmol/L)+40 μmol/L BAI.Each group was treated in triplicate for 24 hours and 48 hours.Cell counting kit-8 (CCK8) was used to detect the inhibitory effect of baicalein; Polymerase chain reaction(PCR) and Western blot were used to analysis the effect of Baicalein on E-cadherin and Vimentin. The expressions of extracellular signal-regulated kinase(ERK), phosphorylated (p-ERK), focal adhesion kinase (FAK) and phosphorylated focal adhesion kinase(p-FAK) were detected by Western blot. The regulatory effect of MEK inhibitor(U0126) on Baicalein was tested by Western blot assay.@*RESULTS@#The survival rate of cells treated with BAI is much lower than that of control group(<0.01); the mRNA and protein levels of E-cadherin were obviously higher than those of control group, while the mRNA and protein levels of Vimentin were lower than those of control group(<0.01).The protein levels of p-ERK and p-FAK treated with BAI were much lower than those of control group(<0.01), but the total ERK and FAK had no obvious changes (<0.05).The protein level of E-cadherin treated with MEK inhibitor was higher than that of control group(<0.01) and the protein levels of Vimentin, p-ERK and p-FAK were lower than those of control group (<0.01), while the total protein levels of ERK and FAK were the same(<0.05).@*CONCLUSIONS@#Baicalein can inhibit the proliferation and invasiveness of OSCC, which may be mediated by ERK-FAK signal pathway.