Fig. 1

The endogenous expression of CEBPA in AML cells is negatively correlated with DDIT3 and cell susceptibility to terminal UPR. A Quantitative PCR analysis of endogenous expression of CEBPA and DDIT3 in AML cell lines. B Correlation analysis using the Pearson model revealed a significant negative correlation between the mRNA levels of CEBPA and DDIT3. (C) Quantitative PCR analysis of endogenous CEBPA and DDIT3 expression in cells from patients with de novo AML and healthy volunteers. Three technical replicates were performed for each sample. (D) The mRNA levels of DDIT3 in primary AML cells were negatively correlated with CEBPA. E–F The CEBPA gene in THP-1 cells, with high endogenous C/EBPα expression and relatively low sensitivity to tunicamycin, was knocked down by shRNA lentiviral vector transfection. The down-regulated level of CEBPA and up-regulated level of DDIT3 were confirmed by quantitative PCR (E) and western immunoblotting analysis (F). G The mRNA levels of several genes encoding proteins in the pro-survival arm of the UPR were decreased after CEBPA knockdown in THP-1 cells. H Compared with the negative control group, THP-1 cells with CEBPA knockdown displayed a significantly increased apoptosis rate after the treatment with tunicamycin (100 ng/ml) for 48 h. Data represent Mean ± SD (n = 3); *P < 0.05; **P < 0.01, ***P < 0.001, ****P < 0.0001