Preliminary Study Of A Retinoid ST1926 On Proliferation And Apoptosis In Human Tongue Squamous Cell Carcinoma Cell Line

ObjectiveThis study investigated the effect of the retinoid ST1926 on antitumor activity.Observe and research the cell proliferation and apoptosis on Tscca(squamous carcinoma cell on human tongue)in vitro.MethodsTsccas were cultured at 37℃ in a 5%CO2condition by RPMI 1640 medium containing 10%FBS(fetal calf serum)and 1% double antibody(penicillin100U/m L,streptomycin 100mg/L),cells were collected in exponential phase.Afterwards the cells were treated with various concentrations of ST1926(0,1,2,3,5,7,15μmol/L)in 24,48,72 hours time-point,detected and analyzed the cell proliferation by MTT(thiazolyl)colorimetric assay.Annexin V and PI double staining united western blotting method was used to detect the rate of the cell early apoptosis,which was treated with various concentrations of ST1926(0,3,5,7μmol/L)in 72 hours time-point.And also the expression levels of caspase3,cleaved-caspase3,caspase7,p-STAT3 and STAT3 were detected.Analyze the possible molecular mechanism of apoptosis in tongue cancer cell line Tscca.Results1.By comparing with the control group,the inhibition rate of cell proliferation was positively correlated with the concentration of ST1926 after stimulating Tscca 24,48,72 hours(P<0.01).The IC50 of ST1926 on Tscca is about2.91μmol/L.2.The early apoptosis rate in the experimental group was significantly higher than that in the control group(P<0.05).There was a negative correlation between the early apoptosis rate and the stimulation concentration(P<0.05).3.After 72 hours time-point,the expression levels of caspase7,cleaved-caspase3,in the experimental group were higher than those in the control group(P<0.05).For p-STAT3,which were lower than those in the control group(P<0.05).There were no significant differents between the experimental group and control group(P>0.05).Conclusions1.The new retinoid ST1926 can inhibit the growth of human tongue squamous carcinoma cell line(Tscca).2.Increasing the apoptosis rate by increasing the cleaved-caspase3 and caspase7 protein expression levels.3.By down regulation the expression levels of the p-STAT3 protein,the mechanism may be related to inhibition the activation of STAT3 protein.