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Detect accessible chromatin using ATAC sequencing in the Kasumi-1 cell line transfected with PHF19 shRNA or scrambled control shRNA

ABSTRACT: To investigate the function of PHF19 in the regulation of chromatin accessibility in t(8;21) AML, we established Kasumi-1 cell line in which PHF19 gene has been knocked down by shRNA. We then performed chromatin accessibility analysis using data obtained from ATAC-seq of the PHF19 knockdown cells and the scrambled control cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE254527 | GEO | 2024/02/05

REPOSITORIES: GEO

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RNA sequencing in the Kasumi-1 cell line transfected with PHF19 shRNA or scrambled control shRNA

Project description:To investigate the fuctional role of PHF19 in the regulation of cell cycle progression in t(8;21) AML, we established Kasumi-1 cell line in which PHF19 gene has been knocked down by shRNA. We then performed bulk RNA sequencing to analyze the changes of gene expression profiling in the PHF19 knockdown cells as compared with the scrambled control cells.

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PHF19 shRNA or scrambled control shRNA

Project description:This SuperSeries is composed of the SubSeries listed below.

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Expression analysis of Kasumi-1 cells treated with or without FTY720

Project description:The clinical outcomes of M2 subtype Acute Myeloid Leukemia (AML-M2) with t(8;21) are poor. Here we report that FTY720 (Fingolimod), a sphingosine analogue and an FDA approved drug for treatment of multiple sclerosis, showed great antitumorigenic activity against Kasumi-1 cell line, xenograft mouse model and leukemic blasts isolated from AML-M2 with t(8;21) patients. Primary investigation indicated that FTY720 caused cell apoptosis through caspase and protein phosphatase 2A (PP2A) activation. Transcriptomic profiling further revealed that FTY720 treatment could upregulate AML1 target genes and interfere with genes involved in ceramide synthesis. FTY720 treatment led to the elimination of AML1-ETO oncoprotein and caused cell cycle arrest. More importantly, FTY720 treatment resulted in rapid and significant increment of pro-apoptotic ceramide levels, determined by HPLC-ESI-MS/MS (high-performance liquid chromatography-electrospray ionization tandem mass spectrometry) based lipidomic approaches. Additionally, structural simulation model indicated that the directly binding of ceramide to inhibitor 2 of PP2A (I2PP2A) could reactivate PP2A and cause cell death. This study demonstrates, for the first time, that accumulation of ceramide plays a central role in FTY720 induced cell death of AML-M2 with t(8;21). Targeting sphingolipid metabolism by using FTY720 may provide novel insight into drug development for AML-M2 treatment. A six chip study using total RNA recovered from three separate cultures of DMSO-treated Kasumi-1 cells and three separate cultures of FTY720-treated Kasumi-1 cells.Each chip measures the expression level of genes from DMSO-/FTY720-treated Kasumi-1 cells.

2014-04-30 | E-GEOD-55772 | biostudies-arrayexpress

Paired ChIP-Seq studies of Kasumi-1 t(8;21) AML cells

Project description:Nearly 10-15% of all acute myeloid leukemia (AML) cases are caused by a recurring chromosomal translocation between 8 and 21, t(8;21). The t(8;21) translocation generates the AML1-ETO leukemia fusion protein. AML1-ETO promotes leukemogenesis by transcriptionally dysregulating important cell-fate genes. Here, to better understand how AML1-ETO deregulates transcription, we performed paired ChIP-Seq analyses of sequence-specific transcription factors, coactivators, corepressors, HDACs, RNA Pol II and acetyl-histone marks in both control and AML1-ETO-depleted Kasumi-1 t(8;21) AML cells.

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Differential cytogenomics and miRNA signature of the Acute Myeloid Leukemia Kasumi-1 cell line CD34+38- compartment

Project description:The t(8;21) Acute Myeloid Leukaemia (AML) Kasumi-1cell line with N822K KIT mutation, is a model system for leukemogenesis. As AML initiating cells reside in the CD34+CD38– fraction, we addressed the refined cytogenomic characterization and miRNA expression of Kasumi-1 cell line and its FACS-sorted subpopulations focussing on this compartment. By conventional cytogenetics, Spectral Karyotyping and array-CGH the cytogenomic profile of Kasumi-1 cells evidenced only subtle regions differentially represented in CD34+CD38– cells.

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miRNA profiling of human acute myeloid leukaemia Kasumi-1 cell line CD34+38- compartment.

Project description:The t(8;21) Acute Myeloid Leukaemia (AML) Kasumi-1cell line with N822K KIT mutation, is a model system for leukemogenesis. As AML initiating cells reside in the CD34+CD38- fraction, we addressed the refined cytogenomic characterization and miRNA expression of Kasumi-1 cell line and its FACS-sorted subpopulations focussing on this compartment. By conventional cytogenetics, Spectral Karyotyping and array-CGH the cytogenomic profile of Kasumi-1 cells evidenced only subtle regions differentially represented in CD34+CD38- cells. Expression profiling by a miRNA platform showed a set of miRNA differentially expressed in paired subpopulations and the signature of miR-584 and miR-182 upregulation in the CD34+CD38- fraction.

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Effect of cabozantinib on transcriptome and signaling pathways in leukemic cell line Kasumi-1

Project description:To identify molecular effects of the tyrosine kinase inhibitor cabozantinib (XL184), we applied gene expression profiling on human acute leukemic cell lines Kasumi-1, which harbors t(8;21) coupled with KIT mutation, by Whole Transcriptome Shotgun Sequencing (RNA-seq). After Kasumi-1 cells were treated with 100nM cabozantinib for 4h or 24h, differentially expressed genes (DEGs) of 124 genes upregulated and 416 were downregulated in 4h, and 184 genes upregulated and 69 genes were downregulated in 24h treatment, compared with vehicle group.

2021-04-22 | GSE153853 | GEO

ATAC-seq analysis of shCtrl and shAML1-ETO Kasumi-1 cells

Project description:Chromatin accessibility was analysed in Kasumi-1 cells after AML1-ETO knock-down and in controls by ATAC-sequencing. The experiments were done in triplicates.

2022-02-01 | E-MTAB-9021 | biostudies-arrayexpress

Phf19 knockdown effect on F9 embryonal carcinoma cells

Project description:PCL family protein Phf19/Pcl3 is one of the accessory components of the PRC2 core complex, and Phf19 is highly expressed in murine ES cells and an ES cell-like embryonic carcinoma cell line, F9 cells. Here we performed microarray analysis of embryonal carcinoma cell line F9 following Phf19 knockdown by shRNA. Knocking down Phf19/Pcl3 in F9 embryonic cells led to derepression of numerous PRC2 direct target genes. 4 sampels including 2 shRNA vector control cell lines and 2 shPhf19 cell lines were used for RNA extraction and Affymetrix mouse 430 2.0 arrays.

2012-12-20 | E-GEOD-42463 | biostudies-arrayexpress

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Project description:miRNA expression profiling of KASUMI-1 ctrl vs KASUMI-1 treated Saha 5 µM 6h

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