Figure 1
From: G9a orchestrates PCL3 and KDM7A to promote histone H3K27 methylation
G9a induces H3K9 and H3K27 methylation and downregulates E-cadherin in pancreatic cancer cells.
(A) Morphology of control, G9a-overexpressing (HPDE-G9a, PANC-1-G9a) cells or G9a-depleted (PANC-1-R-shG9a) cells. (B) Ectopic expression of G9a inhibited E-cadherin expression. The protein levels of G9a and E-cadherin in control and G9a-overexpressing PANC-1 cells were verified by Western blot analysis (top panel) and E-cadherin mRNA level was determined by RT-qPCR analysis. *p < 0.05. (C) PANC-1-R cells transfected with control or various G9a shRNAs were harvested for the analysis of E-cadheirn protein (top panel) and mRNA (low panel). *p < 0.05. (D) PANC-1-R cells were treated with vehicle (DMSO) or UNC0638 (500 nM) for 48 h and the expression of E-cadherin protein and mRNA was investigated. *p < 0.05. (E) PANC-1-R cells were infected with control or G9a shRNA-containing lentivirus. After 48 h, G9a levels and histone methylation status were investigated by Western blot analysis. (F) PANC-1-R cells were infected with control or G9a shRNA-containing lentivirus. ChIP-qPCR analysis was performed to investigate the status of H3K9m2, H3K9m3, H3K27m2 and H3K27m3 in the E-cadherin gene promoter.
