Additional file 1 of Super enhancer related gene ANP32B promotes the proliferation of acute myeloid leukemia by enhancing MYC through histone acetylation

Additional file 1. Figure S1. Western blotting analysis showed that ANP32B protein levels were downregulated in MV4-11 and Kasumi-1 cells after BRD4 knockdown. Figure S2. The knockdown level of ANP32B in MV4-11 and Kasumi-1 cells was verified by qPCR. Figure S3. The knockdown of ANP32B inhibited the growth of MV4-11 cells. A. Monitoring of body weight of the two groups of mice. B. Representative images of H&E staining analysis of liver in two groups of mice. C. Representative images of IHC staining of mice liver. Figure S4. The knockdown of ANP32B inhibited the growth of Kasumi-1 cells. A. Different size and weight of spleen, from sh-NC or sh-ANP32B mices. B. Representative images of IHC staining of mice spleen. Figure S5. IGV visual analysis showed a reduction in H3K27ac signaling in genes involved in the MYC signaling pathway. Figure S6. ANP32B is positively correlated with C-MYC expression. A. Western blotting analysis showed that ANP32B overexpression was established successfully. B. Western blotting analysis showed that ANP32B was positively correlated with C-MYC expression. Table S1. The primer sequences used in this study. Table S2. Super-enhancers identified in each of the 11 AML samples. Table S3. Deferentially expressed genes identified by RNA-Seq of MV4-11 cell after ANP32B knockdown. Table S4. Deferentially expressed genes identified by RNA-Seq of Kasumi-1 cell after ANP32B knockdown. Table S5. In the control group, peaks called by ChIP-Seq of H3K27ac in MV4-11 cell. Table S6. In the ANP32B knockdown group, peaks called by ChIP-Seq of H3K27ac in MV4-11 cell.