Inhibitory effect of lumbrokinase on proliferation and induction on apoptosis of gastric cancer sgc7901 cells / 吉林大学学报(医学版)

ABSTRACT

Objective: To investigate the regulatory effect of lumbrukinase CI.RK) on the gastric cancer SGC7901 Cells, and to clarify its mechanism Methods: The SGC7901 cells in the logarithmic growth phase were selected and divided into control group and 2, 4 , 8 U • ml. I.RK groups. MTT assay was used to detect the inhibitory rates of proliferation of SGC7901 cells in various groups in vitro at different time (24, 48 and 72 h). Cell scratch assay was used to detect the migration abilities of the SGC7901 cells in vitro in various groups. Flow cytometry was used to determine the apoptotic rates of SGC7901 cells and the pencentages of cells at different cell cycles in various groups. The expression levels of Bcl-2, Rax, and caspase-3 in the SGC790I cells in various groups were detected by Western blotting method. Results: The results of MTT assay showed that compared with control group, the inhibitory rates of SGC7901 cells in different doses of I.RK groups after treated for 24, 48 and 72 h were increased ( P<0.01). The cell scratch assay results showed that compared with control group, the migration distances of SGC790I cells in 4 and 8 U • mL"1 I.RK groups were increased significantly ( Pflow cytometry results showed that compared with control group, the apoptotic rates of SGC7901 cells in 4 and 8 U • ml. I.RK groups were increased significantly ( P<0. 01); tlie percentages of cells in Gi and S phases were decreased ( P<0. 01 ); the percentages of cells in G Phase were increased ( P-"C0. 01). The results of Western blotting method showed that compared with control group, the Bcl-2 protein expression level in theSGC7901 cells in 8 U • ml. I.RK group was decreased ( P< 0. 05) ; the Rax and caspase-3 protein expression levels were increased ( P<-'0. 05).

Conclusion:

I.RK can inhibit the proliferation and migration abilities of SGC7901 cells in vitro and induce the apoptosis; its mechanism is achieved through the regulation of expression levels of Rcl-2, Rax, and caspase-3 proteins.