Effects of endogenous reactive oxygen species on migration and invasion of gastric cancer SGC-7901 cells
Objective To investigate the effect of endogenous reactive oxygen species(ROS)on the migration and invasion of gastric cancer SGC-7901 cells.Methods Different concentrations of lipopolysaccharide(LPS)were used to induce cells to produce ROS,and the survival rate of SGC-7901 cells was detected by MTT assay;the intracellular ROS level was detected by fluorescence chemiluminescence;Cell scratch assay and Transwell assay were used to detect the migration and invasion of SGC-7901 cells;the protein expression of copper zinc superoxide dismutase(Cu/Zn-SOD)was detected by Western blot.Based on the presence or absence of intracellular NADPH oxidase inhibitors diphenyleneiodonium chloride(DPI)acting on the cells,the experiment was divided into four groups:control group,LPS group,DPI group and LPS+DPI group.All data were analyzed by SPSS17.0.Results LPS could promote the proliferation of SGC-7901 cells,and the proliferation of SGC-7901 cells was concentration and time-dependent when the concentration of LPS was 500ng/mL,when the concentration of LPS was greater than 500ng/mL,the proliferation of SGC-7901 cells was weakened and the time-dependent effect was not obvious.Over time,the ROS levels in SGC-7901 cells also increased.The ROS level,cell scratch healing rate,and the number of SGC-7901 cells that migrated longitudinally and invaded and penetrated the membrane in the LPS group were higher(faster or more)than those in the control group,DPI group and LPS+DPI group,with statistical significances(P<0.01).The expression level of Cu/Zn-SOD protein in the LPS group was significantly lower than that in the other groups(P<0.01).Conclusion Endogenous reactive oxygen species can promote the migration and invasion of gastric cancer SGC-7901 cells.Inhibiting the level of endogenous reactive oxygen species can slow down the migration and invasion of gastric cancer SGC-7901 cells.
Gastric cancerReactive oxygen speciesLipopolysaccharideCell migration and invasion