Effect of microRNA-32 on the proliferation and migration of gastric cancer cells / 中华消化杂志

ABSTRACT

Objective To explore the effect of microRNA-32 (miRNA-32)on the biological behaviors of gastric cancer cell and its mechanism.Methods Gastric cancer cell line SGC-7901 cells were transiently transfected with miRNA-32 analogue,miRNA-32 inhibitor and empty plasmid vectors by lipofectamine and divided into analogue transfection group,inhibitor transfection group,empty plasmid transfection group and non-transfection group.The expression of green fluorescent protein was observed under fluorescent microscopy.The expression of miRNA-32 at mRNA level was detected by quantificational real-time polymerase chain reaction.The cell proliferation was evaluated by CCK-8 assay.The cell migration ability was measured by scratch test and Transwell chamber assays.The data were analyzed by one-way ANOVA.Results Compared with empty plasmid transfection group and non-transfection group,the expression of miRNA-32 mRNA of miRNA-32 analogue transfection group (relative quantitative value2.327) was significantly up-regulated and that of miRNA-32 inhibitor transfection group (relative quantitative value0.402) was significantly down regulated (F=11.238,P＜0.05).The width of scratch of miRNA-32 analogue transfection group was (61.39± 2.21) μm at 24 hours; miRNA-32 inhibitor transfection group was (29.97±0.66) μm.The migration distance of inhibitor transfection group was far than that of analogue transfection group (F=9.371,P＜0.05).After transfection for 48 hours,the cell number of migrated cells of analogue transfection group was significantly less than that of non transfection group,which was 16.93±4.63 and 93.93± 7.09,respectively (F=6.853,P＜0.05).After transfection for 48 hours and 72 hours,the cell growth inhibiting rate of miRNA 32 analogue transfection group was (43.474 ± 18.636)％ and (45.050±23.764)％,respectively,the cell growth was significantly inhibited (F=7.986 and 8.635,P=0.028 and 0.032).Conclusion The cell growth and migration ability of human gastric cancer cell line SGC-7901 are obviously inhibited through upregulating the expression of miRNA-32.