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Effect of genom-wide depletion on gene expression during treatment with the JAK2 inhibitor Ruxolitinib of JAK2 mutated HEL erythroleukemia cells [CRISPR]

ABSTRACT: Effect of genom-wide depletion on gene expression during treatment with the JAK2 inhibitor Ruxolitinib of JAK2 mutated HEL erythroleukemia cells [CRISPR]

PROVIDER: PRJNA838373 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19215710_1.fastq.gz	Fastqsanger.gz
	SRR19215710_2.fastq.gz	Fastqsanger.gz
	SRR19215711_1.fastq.gz	Fastqsanger.gz
	SRR19215711_2.fastq.gz	Fastqsanger.gz
	SRR19215712_1.fastq.gz	Fastqsanger.gz

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Effect of genom-wide depletion on gene expression during treatment with the JAK2 inhibitor Ruxolitinib of JAK2 mutated HEL erythroleukemia cells [CRISPR]

Project description:In order to confirm the functional dependency on KDM4C under treatment conditions with the JAK-inhibitor ruxolitinib (RUX), we applied a genome-wide CRISPR-Cas9 screen in the human JAK2-mutated cell line HEL by CRISPR/Cas9.

2022-05-18 | GSE203059 | GEO

Effect of depletion of KDM4C on gene expression of JAK2-mutated HEL erythroleukemia cells [RNA-seq]

Project description:Effect of depletion of KDM4C on gene expression of JAK2-mutated HEL erythroleukemia cells [RNA-seq]

| PRJNA838374 | ENA

Expression data of HEL cells with or without LY2784544 and GRN163L

Project description:The mutant JAK2v617F is a driver of myeloproliferative neoplasms(MPNs). Consequently, several JAK2 inhibitors are currently being studied in clinical trials. The most investigated JAK2 inhibitor, Ruxolitinib, provides significant and sustained improvements in spleen related and constitutional symptoms secondary to the disease and represents a milestone in the treatment of myelofibrosis. However, JAK2 inhibitors are non-curative and murine experiments have shown that JAK2 inhibitors don?t eradicate MPN stem cells. In the present study, we determined the effect of the specific JAK2V617F inhibitor LY2784544 on leukemic stem (CD34+) cells (LSCs) using the JAK2V617F-bearing erythroleukemia cell line HEL. The LY2784544 treatment caused a transient proliferation inhibition and apoptosis of HEL cells, but a recovery occurred within a week. Thereafter, the continuous exposure of HEL cells to LY2784544 induced the accumulation of CD34+ LSCs, and the CD34+ cell fraction increased from 8% to over 90% by week 9, which was accompanied by substantially increased clonogenic potentials. A whole-transcript expression analysis revealed a significantly enhanced expression of the stem cell factor KLF4 in LY2784544 treated HEL cells. Inhibiting KLF4 expression attenuated LY2784544-mediated accumulation of CD34+ LSCs. Moreover, we further identified that the telomerase inhibitor GRN163L abolished the LY2784544-mediated CD34+ cell enrichment. Our findings collectively suggest that JAK2 inhibitors may cause enrichment of LSCs and are therefore unlikely to cure MPN as a monotherapy. Moreover, simultaneously targeting JAk2V617F and KLF4 or telomerase may be a novel strategy for MPN treatment.

2019-12-07 | GSE141602 | GEO

Effect of depletion of KDM4C on gene expression of JAK2-mutated HEL erythroleukemia cells [RNA-seq]

Project description:To investigate the function of KDM4C in progression of leukemia, we established HEL-Cas9 cell lines in which the target gene has been knocked out by CRISPR/Cas9. We then performed transcriptome analysis using data obtained from RNA-seq of control or KDM4C depletd cells.

2022-05-18 | GSE203060 | GEO

Comparative gene expression profiling of MHH-CALL4 cells subject to pharmacological JAK2 inhibitor treatment (ruxolitinib or CHZ868) or shRNA-mediated JAK2 depletion in vitro

Project description:Gene expression profiling was performed to characterise transcriptional programs associated with response to type I JAK2 inhibitor ruxolitinib, type II JAK2 inhibitor CHZ868 or shRNA-mediated JAK2 knockdown in MHH-CALL4 cells.

2018-05-31 | GSE102534 | GEO

AG221 and Ruxolitinib Treatment Effects on LSKs in IDH2-R140Q JAK2-V617F Transplant Recipients

Project description:Transplant recipients of IDH2-R140Q JAK2-V617F expressing bone marrow were treated with AG221 and ruxolitinib monotherapy, combined therapy, or vehicle. LSKs were sorted from terminal samples and sequenced with three WT controls.

2018-02-22 | GSE95771 | GEO

Genome-wide occupancy of LSD1 in HEL human erythroleukemia cell line.

Project description:Genome-wide occupancy of LSD1 in HEL human erythroleukemia cell line.

| PRJNA607086 | ENA

PolyA RNA sequencing of HEL human erythroleukemia cell line under LSD1 inhibition

Project description:PolyA RNA sequencing of HEL human erythroleukemia cell line under LSD1 inhibition

| PRJNA607075 | ENA

Integrated genomic analysis illustrates the central role of JAK-STAT pathway activation in myeloproliferative neoplasm pathogenesis [HEL cell lines]

Project description:We used expression profiling, SNP arrays, and mutational profiling to investigate a well-characterized cohort of MPN patients. MPN patients with homozygous JAK2V617F mutations were characterized by a distinctive transcriptional profile. Notably, a transcriptional signature consistent with activated JAK2 signaling is seen in all MPN patients regardless of clinical phenotype or mutational status. In addition, the activated JAK2 signature was present in patients with somatic CALR mutations. Conversely, we identified a gene expression signature of CALR mutations; this signature was significantly enriched in JAK2-mutant MPN patients consistent with a shared mechanism of transformation by JAK2 and CALR mutations. We also identified a transcriptional signature of TET2 mutations in MPN patent samples. Our data indicate that MPN patients, regardless of diagnosis or JAK mutational status are characterized by a distinct gene expression signature with upregulation of JAK-STAT target genes, demonstrating the central importance of the JAK-STAT pathway in MPN pathogenesis. [HEL cell lines] We have performed gene expression profiling in the JAK2V617F homozygous mutant HEL cell line following treatment with 2 independent shRNAs targeting JAK2 or 2 different control shRNAs

2014-06-03 | E-GEOD-54645 | biostudies-arrayexpress

SPAG9-JAK2 gene expression array in Ba/F3 cells

Project description:SPAG9-JAK2 is a novel fusion gene identified in a pediatric patient with Philadelphia chromosome-like acute lymphoblastic leukemia (Ph-like ALL). In this study, we performed functional analysis of the SPAG9-JAK2 fusion to establish molecular targeted therapy. Ba/F3 cells expressing SPAG9-JAK2 generated by retroviral transduction (Ba/F3-SPAG9-JAK2), proliferated in the absence of IL-3, and exhibited constitutive phosphorylation of the tyrosine residues in the JAK2 kinase domain of the fusion protein and STAT3/STAT5. Mutation of tyrosine residues in the JAK2 kinase domain (SPAG9-JAK2 mut) abolished IL-3 independence, but had no influence on STAT3/STAT5 phosphorylation levels. Gene expression analysis revealed that Stat1 was significantly up-regulated in Ba/F3-SPAG9-JAK2 cells. STAT1 was also phosphorylated in Ba/F3-SPAG9-JAK2 but not SPAG9-JAK2 mut cells, suggesting that STAT1 is key for SPAG9-JAK2-mediated cell proliferation. Consistently, STAT1 induced expression of the anti-apoptotic proteins, BCL-2 and MCL-1, as did SPAG9-JAK2, but not SPAG9-JAK2 mut. Ruxolitinib abrogated Ba/F3-SPAG9-JAK2-mediated proliferation in vitro, but was insufficient in vivo. Venetoclax (a BCL-2 inhibitor) or AZD5991 (an MCL-1 inhibitor) enhanced the effects of ruxolitinib on Ba/F3-SPAG9-JAK2 in vitro. These findings suggest that activation of the JAK2-STAT1-BCL-2/MCL-1 axis contributes to SPAG9-JAK2-related aberrant growth promotion. BCL-2 or MCL-1 inhibition is a potential therapeutic option for B-ALL with SPAG9-JAK2 fusion.

2021-05-18 | GSE174578 | GEO

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