Fig. 2

The expression levels of C12orf59 influence the aggressive capacity in vitro and metastasis in vivo. a Western blotting shows that the levels of C12orf59 were largely decreased by the treatment with C12orf59-shRNA-1 or C12orf59-shRNA-2 in MKN-45 and AGS cells, while potentially increased in HGC-27/C12orf59 cell line. b C12orf59 deletion dramatically reduced the migratory ability of GC cells in a wound-healing assay. c Wound-healing assays demonstrate that HGC-27/C12orf59 cells had higher motility than that in HGC-27/vector cells. d Downregulation of C12orf59 resulted in a decrease in the migratory and invasive abilities of GC cells as determined by Transwell analysis. e Overexpression of C12orf59 in HGC-27 cells increased their migratory and invasive abilities. f Representative hematoxylin and eosin (H&E) staining depicting metastatic tumors in the lung of nude mice that originated from MKN-45/shC12orf59 and MKN-45/shcontrol cells injected via the tail vein (left). Number of metastatic nodules formed in the lung of mice 6 weeks after tail vein injection of MKN-45/shC12orf59 or MKN-45/shcontrol cells. Six mice per group; *P < 0.01. g H&E staining depicting metastatic tumors in the lung of nude mice that originated from HGC-27/vector and HGC-27/C12orf59 cells injected via the tail vein (left). Number of metastatic nodules formed in the lung of mice 6 weeks after tail vein injection of HGC-27/vector or HGC-27/C12orf59 cells. Six mice per group; *P < 0.01