Fig. 6
Cyclin G2 inhibits the gastric cancer proliferation and migration hrough Wnt/β-catenin signaling. a-e SGC-7901 cells were infected with cyclin G2 recombinant lentiviruses (LV-cyclin G2) or negative control lentivirus (LV-GPF) for 42 h and then treated with CHIR99021 or DMSO as a negative vehicle control. a and b The infection efficiency of recombinant lentivirus was confirmed by measurement of GFP vector expression (Original magnification, × 200) and western blot analysis of cyclin G2. c Cell lysates were subjected to immunoblot analysis to measure β-catenin protein expression level. d The cell proliferation of SGC-7901 cells was measured by the MTS assay (n = 6). *P < 0.05; **P < 0.01. e The cell migration of SGC-7901 cells was measured by Transwell® migration assays. The data were presented as migrated cells as a percentage of the controls cells at the indicated time-points (n = 3). *P < 0.05; **P < 0.01. f-k AGS cells were overexpressed or knockdown of cyclin G2. f Cell lysates were subjected to immunoblot analysis to determine β-catenin protein expression level in cyclin G2 overexpression or knockdown AGS cells compared with negative control. g MTS cell proliferation assay, (i and j) colony formation assay and (k and l) Transwell® migration assay in cyclin G2 overexpression or knockdown AGS cells compared with the negative control (n = 3). h Cell cycle distributions were detected by flow cytometry analysis in cyclin G2 overexpression AGS cells compared with the negative control (n = 3). *P < 0.05; **P < 0.01