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Objective To detect the effect of oridonin(ORI)on the gene expression of human esophageal carcinoma cell SHEEC and to screen the tumor cell apoptosis target genes.Methods The gene expression of human esophageal carcinoma cell SHEEC without and with ORI induction for 1 hours and 8 hours were detected with microarray technique,respectively.The differentially expressed genes were identified and verified with fluorecent quantitative PCR.Results A total of 1011 genes showed up or down regulation more than twice after ORI induction(including 280 genes after 1 hour and 731 genes after 8 hours induction respectively).In these genes,17 genes with the top extent of up or down regulation were identified,which were involved in the cell signal transduction,transcription regulation,and cell apoptosis.These 17 differentially expressed genes were verified with real-time PCR,and 12 genes were statistically significant.Conclusion In the 12 differentially expressed genes with statistically significance,there may have tumor cell apoptosis target genes induced by ORI through mitochondrion route.
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Aim To study the effects of selective cyclooxygenase-2 (COX-2) inhibitor,nimesulide,on COX-2 expression, cell proliferation and apoptosis of human esophageal carcinoma Eca-109 cell lines. Methods MTT assay was used to observe the proliferative effect;COX-2 mRNA expression was evaluated with RT-PCR; COX-2 protein expression,cell cycle and apoptosis were analyzed with flow cytometry;microscope and agarose gel electrophoresis of DNA were also used to observe the apoptosis. Results Nimesulide significantly inhibited the proliferation of Eca-109 cell lines in a time and dose-depenent fashion, down-regulated the expression of COX-2 mRNA and COX-2 protein in a dose-dependent fashion;nimesulide also decreased the proliferation index and the proportion of cells in S phase, meanwhile increased the proportion of cells in G_0/G_1 phase and induced apoptosis. Conclusion COX-2 selective inhibitor nimesulide inhibits proliferation,induces apoptosis and cell cycle arrest of human esophageal cells via down-regulation of COX-2 expression.
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Objective To investigate the effects and possible mechanisms of ursolic acid (UA) on inhibiting proliferation of human esophageal carcinoma cell Eca-109 and inducing its apoptosis. Methods Cell proliferation was determined by MTT assay. Electron microscope was used to observe the ultrastructural changes of Eca-l09 induced by UA. Cell cycle and apoptotic rate were analyzed by flow cytometry (FCM),and the expression of P27kip1,Bcl-2 and Bax were detected by Western blot method. Results UA could significantly inhibit the growth of Eca-109 cells(P
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Objective Effect of baohuoside-Ⅰ from Cortex Periplocae on cell cycle of human esophageal carcinoma cell Eca-109 and its mechanism were studied.Methods After treatment with baohuoside-Ⅰ at different concentration(12.5,25,and 50 ?g/mL)for 24,48,and 72 h,the inhibitory effect on proliferation of Eca-109 cells was analyzed by MTT method.After treatment with baohuoside-Ⅰ under different concentration(12.5,25,and 50 ?g/mL)for 48 h,cell cycle of Eca-109 cells were measured with flow cytometry(FCM);The expression of Cyclin B1 mRNA was detected by RT-PCR technique.The expression of Cyclin B1 protein was detected by Western blotting.Results Baohuoside-Ⅰ of 25 and 50 ?g/mL inhibited the proliferation of Eca-109 cells significantly in an effect-concentration manner(P