Objective: To investigate the effects of miR-106b on malignant characteristics of gastric cancer cells, andexplore possible mechanisms. Methods: Expression of miR-106b, p21 and E2F was determined by real-timePCR. Transfection with miR-106b mimics was conducted, and gastric cancer cells with miR-106b overexpressionwere obtained. Cells transfected with mimic mutants and those without transfection served as negative andblank controls, respectively. Flow cytometry and transwell assays were adopted to detect the effects of miR-106boverexpression on cell cycle, migration and invasion of gastric cancer cells. Results:. The expression of miR-106b in gastric cancer cells was significantly higher than that in normal gastric mucosa cells. Furthermore, theexpression level of miR-106b rose according to the degree of malignacy among the three GC cell strains (MKN-45 > SGC-7901 > MKN-28). Overexpression of miR-106b shortened the G0/G1 phase and accelerated cell cycleprogression, while reducing p21 and E2F5, without any significant effects on the capacity for migration andinvasion of gastric cancer cells. Conclusions: miR-106b may promote cell cycling of gastric cancer cells throughregulation of p21 and E2F5 target gene expression.
(2013). Effects of MicroRNA-106 on Proliferation of Gastric Cancer Cell through Regulating p21 and E2F5. Asian Pacific Journal of Cancer Prevention, 14(5), 2839-2843.
MLA
. "Effects of MicroRNA-106 on Proliferation of Gastric Cancer Cell through Regulating p21 and E2F5". Asian Pacific Journal of Cancer Prevention, 14, 5, 2013, 2839-2843.
HARVARD
(2013). 'Effects of MicroRNA-106 on Proliferation of Gastric Cancer Cell through Regulating p21 and E2F5', Asian Pacific Journal of Cancer Prevention, 14(5), pp. 2839-2843.
VANCOUVER
Effects of MicroRNA-106 on Proliferation of Gastric Cancer Cell through Regulating p21 and E2F5. Asian Pacific Journal of Cancer Prevention, 2013; 14(5): 2839-2843.