OBJECTIVE: To investigate the effects of miR-106b on malignant characteristics of gastric cancer cells, and explore possible mechanisms. METHODS: Expression of miR-106b, p21 and E2F was determined by real-time PCR. Transfection with miR-106b mimics was conducted, and gastric cancer cells with miR-106b overexpression were obtained. Cells transfected with mimic mutants and those without transfection served as negative and blank controls, respectively. Flow cytometry and transwell assays were adopted to detect the effects of miR-106b overexpression 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, the expression 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 cycle progression, while reducing p21 and E2F5, without any significant effects on the capacity for migration and invasion of gastric cancer cells. CONCLUSIONS: miR-106b may promote cell cycling of gastric cancer cells through regulation of p21 and E2F5 target gene expression.
OBJECTIVE: To investigate the effects of miR-106b on malignant characteristics of gastric cancer cells, and explore possible mechanisms. METHODS: Expression of miR-106b, p21 and E2F was determined by real-time PCR. Transfection with miR-106b mimics was conducted, and gastric cancer cells with miR-106b overexpression were obtained. Cells transfected with mimic mutants and those without transfection served as negative and blank controls, respectively. Flow cytometry and transwell assays were adopted to detect the effects of miR-106b overexpression 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, the expression 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 cycle progression, while reducing p21 and E2F5, without any significant effects on the capacity for migration and invasion of gastric cancer cells. CONCLUSIONS:miR-106b may promote cell cycling of gastric cancer cells through regulation of p21 and E2F5 target gene expression.
Authors: Estefanía Lozano-Velasco; Daniel Vallejo; Francisco J Esteban; Chris Doherty; Francisco Hernández-Torres; Diego Franco; Amelia Eva Aránega Journal: Mol Cell Biol Date: 2015-06-08 Impact factor: 4.272
Authors: Hang Tian; Lei Hou; Yu-Mei Xiong; Jun-Xiang Huang; Wen-Hua Zhang; Yong-Ying Pan; Xing-Rong Song Journal: Am J Transl Res Date: 2016-03-15 Impact factor: 4.060