Fig. 8From: Upregulation of SNTB1 correlates with poor prognosis and promotes cell growth by negative regulating PKN2 in colorectal cancerSNTB1 knockdown suppresses cell proliferation and induces cell apoptosis dependent on PKN2. HCT116 cells were transfected with si-SNTB1 or si-PKN2, or combination of si-SNTB1 and si-PKN2, or their related control siRNA (si-Ctrl). a The protein levels of SNTB1 (left) and PKN2 (right) in HCT116 cells were determined by Western-blot analysis. The representative images of PKN2, SNTB1 and GAPDH were shown and were quantitated using ImageLab software. GAPDH was used as an internal control and normalized to GAPDH. *P < 0.05, #P < 0.05 vs. si-PKN2. b The cell viability of CRC cells was determined by the CCK-8 assay. The cell viability in si-Ctrl was set as 1. Data were normalized to the viability of si-Ctrl and represented as the fold change. *P < 0.05 vs. si-Ctrl, #P < 0.05 vs. si-PKN2. c The colony formation assay was performed to determine cell survival. The images were taken and the number of colonies were calculated and normalized to the survival of control cells. *P < 0.05, #P < 0.05 vs. si-PKN2. d The cell cycle progression in HCT116 cells was determined by PI staining and FACS analysis. Representative plots (left panels) and percentage of cells (right panel) at different stages (G0/G1, G2/M and S phases) are presented. *P < 0.05. e Apoptosis of HCT116 cells was determined by Annexin V staining and FACS analysis. Representative plots (left panels) and percentage of apoptotic cells (right panel) are presented. *P < 0.05Back to article page