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HUANG Guo, WANG You-quan, LIU Guo-wen.et al, . Mechanism of curcumin-induced apoptosis of gastric cancer SGC-7901 cells[J]. Chinese Journal of Public Health, 2017, 33(7): 1082-1085. DOI: 10.11847/zgggws2017-33-07-13
Citation: HUANG Guo, WANG You-quan, LIU Guo-wen.et al, . Mechanism of curcumin-induced apoptosis of gastric cancer SGC-7901 cells[J]. Chinese Journal of Public Health, 2017, 33(7): 1082-1085. DOI: 10.11847/zgggws2017-33-07-13

Mechanism of curcumin-induced apoptosis of gastric cancer SGC-7901 cells

  • Objective To explore possible mechanism of curcumin-induced apoptosis of human gastric cancer SGC-7901 cells.Methods Human gastric cancer SGC-7901 cells were cultured in vitro.Cell counting kit-8 (CCK-8) was used to evaluate anti-proliferative effect of curcumin at different concentrations on SGC-7901 cells;flow cytometry was adopted to assess cell cycle of the SGC-7901 cells.The expressions of nuclear factor-kappa B (NF-κB),livin and caspase-3 in SGC-7901 cells were determined with Western blot.Results Compared with that of the control group,the proliferation of SGC-7901 cells treated with different doses of curcumin was inhibited in dose-dependent (r=0.901,P<0.01) and time-dependent manner (r=0.389,P<0.01).Compared with that (2.8%) of the control group,the apoptosis rate of SGC-7901 cells treated with 20,40,and 60 μmol/L curcumin were significantly higher (7.7%,13.4%,and 7.7%;P<0.05 for all).Compared with that (58.59%) of the control group,the proportion of cells arrested in G1 phase for the SGC-7901 cells treated with 20,40,and 60 μmol/L curcumin were significantly higher (60.24%,65.13%,and 68.35%;P<0.05 for all).Compared with those of the control group,significantly decreased expression of NF-κB and livin and increased expression of caspase-3 protein were observed in SGC-7901 cells treated with curcumin in a dose-effect manner (P<0.05 for all).Conclusion Curcumin inhibits the activity of gastric cancer SGC-7901 cells and the mechanism of the effect may be related to the induction of cell apoptosis due to decreased NF-κB and the promotion of livin's inhibition effect on caspase and the activation of caspase-3.
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