| Objective:This study is intended to investigate the relationship between proliferation and apoptosis of the cervical cancer cell affected by cisplatin and IGF-1R, by way of intervening in cervical cancer Hela and Caski cell strains with cisplatin to affect cancer cell proliferation and apoptosis, IGF-1R expression levels.Method:(1) Produce human cervical cancer cell strains--Hela cell and Caski cell, by means of vitro culture; (2) Test the effects of the intervention by cisplatin with different concentrations on growth and proliferation of cervical cancer cell with MTT chromometry; (3)Detect the impacts of cisplatin with different concentrations on cervical cancer apoptosis with AO fluorescence staining; (4)Test the differences of IGF-1R protein expression before and after the intervention of cisplatin with different concentrations through immunocytochemistry.Result:(1) MTT results show that during the same acting time, the two groups of cells'survival rate decreases gradually as the chemical concentration increases; especially the growth inhibition of the groups under the intervention of cisplatin of 4ug/ml,2ug/ml, with statistical difference (P<0.01), is the most obvious. The survival rate of cell groups under the intervention of 0.25ug/ml,0.125ug/ml and DMSO has no significant difference (P> 0.05). Their survival rates are much higher than that of groups with different concentrations, which produces statistical significance (P<0.01). The survival rate of cells under the intervention of lug/ml and 0.5ug/ml has no significant difference (P> 0.05). Under the intervention of the same acting time and the same dose of drug, Caski cells'survival rate is slightly higher than Hela group, but neither has statistical difference (P> 0.05). Within different acting time, the DMSO group of the two groups showes no significant difference (P> 0.05). (2) The testing result of AO fluorescence staining shows that: under the intervention of different concentrations of DDP, the apoptosis rates of Hela and Caski are different in different time. The apoptosis rates increase obviously as DDP dose increases or the acting time extends, and both of them have significant difference (P<0.01). Under the intervention of the same DDP dose within the same acting time, Caski group's apoptosis rate is lower than that of Hela group, and both have statistical difference (P<0.05). When making comparison in the same time period, the apoptosis rates of DMSO group in various periods show no significant difference (P> 0.05). The apoptosis rates of both groups are markedly increased after the DDP concentration exceeds 0.25ug/ml(P<0.01).(3) Immunocytochemistry results show that:IGF-1R protein make high expression in cervical carcinoma cell strain; under the intervention of the same DDP dose within the same acting time, IGF-1R protein expression of Caski cells is higher than that of Hela cells, and IGF-1R protein expression will decrease with greater DDP concentration and longer acting time. Within different acting time, the difference between IGF-1R expression in the control group PBS has no statistical significance (P> 0.05); IGF-1R protein expression in PBS control group is significantly higher than other groups, which has statistical significance (P<0.01); IGF-1R protein expression in the 4μg/ml group is significantly lower than other groups, and the difference has statistical significance (P<0.01). IGF-1R protein expression shows dose-dependent decline, and the difference among the groups is statistically significant (P<0.01).(4) Bivariate correlation analysis show that:IGF-1R protein expression level is positively correlated with survival rate of the two cell groups (P<0.01), and it is negatively correlated with apoptosis rate of the two groups (P<0.01).Conclusions:(1) There may be a connection between high expression of IGF-1R and the incidence of cervical cancer; and IGF-IR expression in squamous carcinoma cells maybe higher than in adenocarcinoma cells.(2) Perhaps cisplatin inhibits cancer cells proliferation and apoptosis through reducing the expression of IGF-1R. |