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ISSN 1001-5256 (Print)
ISSN 2097-3497 (Online)
CN 22-1108/R
Issue 12
Dec.  2018
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Effect of cyclooxygenase-2 antisense RNA combined with celecoxib on the proliferation and apoptosis of hepatoma cells

DOI: 10.3969/j.issn.1001-5256.2018.12.021
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  • Published Date: 2018-12-20
  • Objective To investigate the antitumor effect of cyclooxygenase-2 (COX-2) antisense RNA combined with celecoxib on hepatoma CBRH7919 cells. Methods The effect of celecoxib on in vitro proliferative activity, cell cycle, and apoptosis of hepatoma cell lines CBRH7919, CBRH7919-E, and CBRH7919-A (transfected with COX-2 antisense gene segment) were observed. MTT assay, cell cycle analysis, and RT-PCR were used to evaluate the change in in vitro proliferation of hepatoma cell lines. A multivariate analysis of variance was used for comparison of continuous data between groups, and the SNK-q test was used for further comparison between two groups.Results After the treatment with celecoxib, CBRH7919-A cells had a significant reduction in growth rate compared with CBRH7919 and CBRH7919-E cells (F = 38. 303, P < 0. 01) , in a time-and dose-dependent manner (F = 162. 638 and 22. 666, both P < 0. 01) .Celecoxib significantly increased the proportion of cells in G0/G1 phase and had a marked inhibitory effect on cells in S phase in a dose-dependent manner (F = 32. 515, P < 0. 01) , while there was no significant change in the proportion of cells in G2/M phase. Compared with CBRH7919 and CBRH7919-E cells, CBRH7919-A cells were more sensitive to celecoxib (F = 1219. 506, P < 0. 01) . After the treatment with celecoxib at different concentrations (40 and 80 μmol/L) , all three groups had a significant increase in cell apoptosis (all P <0. 01) , and there was no significant difference in apoptosis between the three groups (P > 0. 05) . Conclusion COX-2 antisense RNA combined with celecoxib can inhibit the in vitro growth and proliferation and cell cycle of hepatoma CBRH7919 cells, promote apoptosis, and thus exert a potential therapeutic effect on hepatoma cells.

     

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