Fig. 2
KRT16 regulates migration, invasion, sphere formation, and the metastatic abilities of OSCC cells. a The expression levels of KRT16 in two series of in vivo selected highly invasive lines (C9 pair and OC-3 pair) were measured through qRT-PCR (left) and immunoblotting (right). The actin was used as an internal control. b Left, the inhibitory efficacy of three specific KRT16-siRNAs. Right, immunoblotting of KRT16 protein in OC-3-IV cells transfected with the KRT16-siRNAs or NC-siRNA. c A decrease in migration and invasion abilities was observed in OC-3-IV cells transfected with KRT16-siRNA-3 compared with the control (NC-siRNA). d Left, immunoblotting of KRT16 from OC-3-IV cells transfected with the KRT16 plasmid or control vector. Right, cell migration and invasion were increased through ectopic expression of KRT16 in OC-3-IV cells. e Lung metastasis was reduced following tail vein injection of 1 × 106 OC-3-IV cells transiently transfected with KRT16-siRNA. f Representative xenograft tumors formed by 1 × 103 OC-3-IV sphere cells in the CB17-SCID mice. Tumor growth was monitored through BLI. Representative BLI results are shown at day 40 after implantation. g Sphere-forming ability of OC-3-IV cells was suppressed by KRT16-siRNA and enhanced by KRT16 overexpression. Sphere formation under stem cell selective condition was examined on day 10 after culturing of the cells transfected with the indicated siRNA or KRT16-plasmid. The original magnification was 40x. Histograms represent means ± SD from three independent experiments (*P < 0.05, **P < 0.01)