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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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			Action	DRS
	ERR3632896_1.fastq.gz	Fastqsanger.gz
	ERR3632896_2.fastq.gz	Fastqsanger.gz

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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

2020-06-30 | E-MTAB-8491 | biostudies-arrayexpress

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.

2020-06-30 | E-MTAB-8480 | biostudies-arrayexpress

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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Functional, structural, and molecular characterizations of the leukemogenic driver MEF2D-HNRNPUL1 fusion.

Project description:Recurrent MEF2D fusions with poor prognosis have been identified in B-cell precursor ALL (BCP-ALL). The molecular mechanisms underlying the pathogenic function of MEF2D fusions are poorly understood. Here, we show that MEF2D-HNRNPUL1 (MH) knock-in mice developed a progressive disease from impaired B-cell development at the pre-pro-B stage to pre-leukemia over 10 to 12 months. When cooperating with NRASG12D, MH drove an outbreak of BCP-ALL, with a more aggressive phenotype than the NRASG12D-induced leukemia. RNA-sequencing identified key networks involved in disease mechanisms. In chromatin immunoprecipitation-sequencing experiments, MH acquired increased chromatin-binding ability, mostly through MEF2D-responsive element (MRE) motifs in target genes, compared with wild-type MEF2D. Using X-ray crystallography, the MEF2D-MRE complex was characterized in atomic resolution, whereas disrupting the MH-DNA interaction alleviated the aberrant target gene expression and the B-cell differentiation arrest. The C-terminal moiety (HNRNPUL1 part) of MH was proven to contribute to the fusion protein's trans-regulatory activity, cofactor recruitment, and homodimerization. Furthermore, targeting MH-driven transactivation of the HDAC family by using the histone deacetylase inhibitor panobinostat in combination with chemotherapy improved the overall survival of MH/NRASG12D BCP-ALL mice. Altogether, these results not only highlight MH as an important driver in leukemogenesis but also provoke targeted intervention against BCP-ALL with MEF2D fusions.

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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

Project description:miRNA expression profiling of KASUMI-1 ctrl vs KASUMI-1 treated Saha 5 µM 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.

2022-06-01 | GSE196232 | GEO

Gene expression signatures of MEF2D-silencing hepatocellular carcinoma cells

Project description:Global expression profiles in Huh7 after infection with Lv-shMEF2D and Lv-scrambled, as well as transfection with siRNA-MEF2D and siRNA-control, were compared to investigate the molecular mechanisms involved in MEF2D-mediated regulation of cell cycle. In order to investigate the molecular mechanisms involved in MEF2D-mediated regulation of cell cycle, we assessed gene expression profiles in Huh7 cells after infection with Lv-shMEF2D and Lv-scrambled, as well as transfection with siRNA-MEF2D and siRNA-control, by cDNA microarray. Analysis of global mRNA expression profile indicated a shift toward G2/M arrest in the cells after downregulating MEF2D expression. The genes that inhibit G2/M transition were found to be expressed in high level in MEF2D-downregulated group, as compared with control group. Meanwhile, mRNA abundance of G2/M transition-promoting genes, except CDC2 and CDC25C, was reduced when MEF2D expression was depressed in Huh7 cells

2015-04-07 | E-GEOD-37123 | biostudies-arrayexpress

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