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ATAC-seq of Kasumi-7 acute lymphoblastic leukemia cell line harboring MEF2D-HNRNPUL1 fusion gene

ABSTRACT: ATAC-seq of Kasumi-7 acute lymphoblastic leukemia cell line harboring MEF2D-HNRNPUL1 fusion gene

PROVIDER: PRJEB35179 | ENA |

REPOSITORIES: ENA

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MEF2D-HNRNPUL1 ChIP-seq in a genome-edited Kasumi-7 cell line

Project description:Acute lymphoblastic leukemia harboring the fusion genes involving the MEF2D transcription factor (MEF2D-ALL) is associated with poor clinical outcomes. To explore binding sites in the genome in MEF2D-ALL, we genome-edited a MEF2D-ALL cell line Kasumi-7 so that the fusion is tagged with HA at the carboxyl-terminal and co-expressed with GFP. We used this cell line for ChIP-seq using anti-HA antibody. Pair-end reads for Input and HA ChIP DNA are provided.

2020-06-30 | E-MTAB-8466 | biostudies-arrayexpress

ATAC-seq of Kasumi-7 acute lymphoblastic leukemia cell line harboring MEF2D-HNRNPUL1 fusion gene

Project description:ATAC-seq. was performed to examine open chromatin regions in an acute lymphoblastic leukemia cell line, Kasumi-7

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RNA-seq for gene expression changes upon silencing MEF2D-fusion in a MEF2D-HNRNPUL1 fusion-expressing Kasumi-7 cell line

Project description:To explore the mechanisms underlying the maintenance of acute lymphoblastic leukemia harboring fusion genes involving MEF2D transcription factor, the MEF2D-fusion was silenced by shRNA and the resulting gene expression changes were analyzed by RNA-seq.

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RNA-seq for gene expression changes upon silencing MEF2D-fusion in a MEF2D-HNRNPUL1 fusion-expressing Kasumi-7 cell line

Project description:RNA-seq for gene expression changes upon silencing MEF2D-fusion in a MEF2D-HNRNPUL1 fusion-expressing Kasumi-7 cell line

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MEF2D-HNRNPUL1 ChIP-seq in a genome-edited Kasumi-7 cell line

Project description:MEF2D-HNRNPUL1 ChIP-seq in a genome-edited Kasumi-7 cell line

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Genomic Analyses Identify Recurrent MEF2D Fusions in Acute Lymphoblastic Leukemia

Project description:Chromosomal rearrangements are initiating events in acute lymphoblastic leukemia (ALL). Here, using RNA-sequencing (RNAseq) of 560 ALL cases, we identify rearrangements between MEF2D (myocyte enhancer factor 2D) and five genes (BCL9, CSF1R, DAZAP1, HNRNPUL1 and SS18) in 22 B progenitor ALL (B-ALL) cases with a distinct gene expression profile, the most common of which is MEF2D-BCL9. Examination of an extended cohort of 1164 B-ALL cases identified 30 cases with MEF2D rearrangements which include an additional fusion partner, FOXJ2, thus MEF2D-rearranged cases comprise 5.3% of cases lacking recurring alterations. MEF2D-rearranged ALL is characterized by a distinct immunophenotype, DNA copy number alterations at the rearrangement sites, older diagnosis age, and poor outcome. The rearrangements result in enhanced MEF2D transcriptional activity, lymphoid transformation, activation of HDAC9 expression and sensitive to histone deacetylase inhibitors treatment. Thus, MEF2D-rearranged ALL represents a distinct form of high-risk leukemia, for which new therapeutic approaches should be considered.

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KASUMI-1ctrl vs KASUMI-1 Saha (Vorinostat; suberoylanilide hydroxamic acid) 6h

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Next Generation Sequencing of Wild Type and Hnrnpul1-/- RAW 264.7 Cells Transcriptomes

Project description:Purpose: The goal of this study is to compare NGS-derived wild type and Hnrnpul1 knockout (Hnrnpul1-/-) RAW 264.7 cells transcriptomes with or without LPS stimulation. Methods: Sequancing was performed by Novogene China Co. Ltd. RNA profiles of wild type and Hnrnpul1-/- RAW 264.7 cells as well as LPS stimulated (10 h) wild type and Hnrnpul1-/- RAW 264.7 cells were generated by deep sequencing using Illumina Novaseq 6000. Index of the reference genome was built using Hisat2 v2.0.5 and paired-end clean reads were aligned to the reference genome using Hisat2 v2.0.5. featureCounts v1.5.0-p3 was used to count the reads numbers mapped to each gene. And then FPKM of each gene was calculated based on the length of the gene and reads count mapped to this gene. Method of TMM was used to normalize the readcount. Negative binomial distribution model was used to calculate the P value, and FDR was calculated by the method of Benjaminiand Hochberg. Results: Using an optimized data analysis workflow, we mapped about 40 million sequence reads per sample to the mouse genome (GRCm38/mm10). Comparing to wild type RAW 264.7 cells, 237 genes were up-regulated and 181 genes were down-regulated in Hnrnpul1-/- cells. At 10 h following LPS stimulation, 341 genes were up-regulated and 288 genes were down-regulated in Hnrnpul1-/- cells. Genes were pre-ranked according to log2FoldChange(KO/WT) followed by GSEA and 6 gene sets were significantly enriched. Significantly differential genes were undergone GO analysis (biological process) and biological process including cell-cell adhesion, positive regulation of cell activation and regulation of response to external stimulus were enriched. Conclusions: Lacking Hnrnpul1 promotes the expression of inflammatory cytokines in LPS stimulated RAW 264.7 cells.

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