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Effects And Mechanisms Of TSA On The Proliferation And Apoptosis Of Human BGC 823 Gastric Cancer Cells

Posted on:2017-01-15Degree:MasterType:Thesis
Country:ChinaCandidate:J YaoFull Text:PDF
GTID:2284330503963418Subject:Internal medicine
Abstract/Summary:PDF Full Text Request
Objective:To investigate the effects of trichostatin A (TSA) on apoptosis, growth and proliferation of human gastric cancer BGC823 cells, study effections of TSA on survivin and β-catenin mRNA expression of BGC823 human gastric cancer cells whicn to provide the experimental and theoretical basis for clinical treatment and research of gastric cancer.Methods:Cultivation of BGC823 Human gastric cancer cells in vitro, CCK-8 method for the determination of human gastric cancer BGC823 cell proliferation using different concentrations of drugs interfere different time. The influence of its apoptosis rate was analyzed with flow cytometry (FCM), quantitative real-time PCR was used to compare the mRNA expression of survivin and β-catenin in BGC823 human gastric cancer cells.Results:1. TSA inhibition of BGC823 human gastric cancer cellsThe CCK-8 results showed:TSA inhibit the proliferation of human gastric cancer BGC823 in dose and time dependent manners in vitro. With the increasing of the concentration of TSA (0 nmol/L,100 nmol/L,200 nmol/L,400 nmol/L) and action time (12 h,24 h,48 h), the rate of apoptosis gradually increased, the differences were statistically significant (P<0.05).BGC823 human gastric cancer cell inhibition rate by different concentrations interfer the same time (12h):The inhibition rate is (26.188± 0.209)% when the concentration of TSA is 100 nmol/L. The inhibition rate is (41.326± 0.166)% when the concentration of TSA is 200 nmol/L. The inhibition rate is (45.476± 0.513)% when the concentration of TSA is 400 nmol/L. The inhibition increased when concentration of TSA increased.Fix TS A concentration to 400 nmol/L, with the prolonging of time, the inhibition rate increased gradually. They are (45.476± 0.513)%, (80.014± 0.564)%, (82.246± 0.676)% in 12 h,24 h,48 h respectively.2.TSA induced the apoptosis of BGC823 human gastric cancer cellsThe oncentration of 0 nmol/L,100 nmol/L,200 nmol/L,400 nmol/L TSA intervent BGC823 after 48h respectively, the rate of apoptosis are (1.752± 0.011)%, (1.865± 0.013)%, (33.996± 0.217)%, (44.503± 0.522)%. The concentration of TSA was statistically significance between 200 nmol/L group and 400 nmol/L group VS control group in 48h TSA apoptosis rate experiment. There is no statistical significance of apoptosis rate differences between 100 nmol/L TSA group and control group.3.Quantitative real-time PCR detect the mRNA expression of survivin and β-catenin in BGC823 human gastric cancer cells.Real-time PCR results showed:With TSA concentration increased (0 nmol/L,100 nmol/L, 200 nmol/L,400 nmol/L), the expression levels of survivin and β-catenin gene occurred down, its expression level compared to the control group, the difference was statistically significant (P <0.05).Conclusion:1. TSA can inhibits the proliferation of human gastric cancer BGC823 cell. With the extension of TSA treatment concentration and increasing the time of intervention, its BGC823 human gastric cancer cell inhibition rate gradually increased in a dose-dependent and time-dependent manner (p<0.05).2. When Intervent 48 hours, concentration of TSA higher than 200 nmol/L,it can induce apoptosis in BGC823 human gastric cancer cells.3. TSA inhibits BGC823 human gastric cancer cell proliferation may be associated with reduced the expression of survivin and β-catenin gene’s expression.
Keywords/Search Tags:trichostatin A, gastric cancer, CCK8, apoptosis, survivin, β-catenin
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