Fig. 6

Activation of AKT by CBX7 leads to upregulation of NF-κB activity. a CBX7 overexpression upregulates the expression of phosphorylated P65 (pP65) and increases the expression of phosphorylated AKT (pAkt) in SGC7901 cells (upper panel) . The expression of CBX7, pAKT, total AKT (tAKT), pP65, and P65 was analyzed by Western blot analysis in gastric cancer cells. Treatment with AKT inhibitor LY294002 reduces the expression of pP65 induced by overexpression of mAKT. The lower panel represents normalized ratio of phospho P65/β-act of each group. b CBX7 knockdown downregulates the expression of pP65 and pAKT in SGC7901 cells (upper panel). The expression of CBX7, pAKT, total AKT (tAKT), pP65, and P65 was analyzed by Western blot analysis in gastric cancer cells. Constitutive active form of AKT can increase the expression of pP65 inhibited by CBX7 knockdown. The effect of CBX7 and AKT on pP65 and total P65 expression was determined using Western blot analysis. The lower panel represents normalized ratio of phospho P65/β-act of each group. c Treatment with AKT inhibitor LY294002 suppresses NF-κB transcriptional activity induced by CBX7 overexpression. Transcriptional activity of NF-κB in gastric cancer cells was determined by dual luciferase reporter assay. d AKT activator SC-79 abrogates CBX7 depletion-mediated suppression of NF-κB transcriptional activity. Transcriptional activity of NF-κB in gastric cancer cells was determined using dual luciferase reporter assay. e PI3K inhibitor INK1197 inhibits the expression of miR-21 induced by CBX7 overexpression. Fold change of miR-21 in gastric cancer cells was determined using quantitative RT-PCR analysis. f NF-κB inhibitor PDTC inhibits the expression of miR-21 induced by CBX7 overexpression. Fold change of miR-21 in gastric cancer cells was analyzed using quantitative RT-PCR analysis