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Genetic analysis of Ikaros target genes and tumor suppressor function in BCR-ABL1+ pre-B ALL [RNA-seq]

ABSTRACT: RNA-seq was performed in human Ph+ pre-B ALL cells that harbor a deletion of the Ikaros DNA binding domain (Ik6) after doxycycline induction of exogenous expression of wild-type Ikaros (Ik1) or control empty vector over 0, 12, 24 and 48 hours. Biological replicates (n=2) using independent cultures and inductions were performed.

ORGANISM(S): Homo sapiens

PROVIDER: GSE90659 | GEO | 2017/02/06

SECONDARY ACCESSION(S): PRJNA355295

REPOSITORIES: GEO

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Genetic analysis of Ikaros target genes and tumor suppressor function in BCR-ABL1+ pre-B ALL [ATAC-Seq]

Project description:Using patient-derived Ph+ pre-B ALL cells that harbor deletions of the IKZF1 DNA binding domain (Ik6), we performed ATAC-sequencing in cells that inducibly express wild-type Ikaros (Ik1) or an empty vector control.

2017-02-06 | GSE90666 | GEO

Genetic analysis of Ikaros target genes and tumor suppressor function in BCR-ABL1+ pre-B ALL [ChIP-seq]

Project description:ChIP-seq was performed in patient-derived BCR-ABL1+ (Ph+) pre-B ALL cells that harbor heterozygote deletions of the IKZF1 DNA binding domain (Ik6), using cells that inducibly express wild-type Ikaros (Ik1) or an empty vector control.

2017-02-06 | GSE90656 | GEO

BCR-ABL1 and a dominant negative isoform of Ikaros cooperate to induce human acute myeloid leukemia

2014-05-23 | GSE45452 | GEO

BCR-ABL1 and a dominant negative isoform of Ikaros cooperate to induce human acute myeloid leukemia

Project description:Analysis of lineage depleted human cord blood cells sequentially transduced with retro- (BCR-ABL1) and lentiviral (Ik6) vectors and the corresponding controls. Results provide important informations on the collaboration of BCR-ABL1 and Ik6 in human hematopoietic cells. Double-transduced lineage depleted human cord blood cells were puirifed according to GFP and LNGFR expression. RNA was extracted from purified cells.

2014-05-23 | E-GEOD-45452 | biostudies-arrayexpress

Ikaros-regulated genes in a mouse model of BCR-ABL1+ acute lymphoblastic leukemia

Project description:To examine Ikaros tumor suppressor mechanisms, we have utilized inducible RNAi to dynamically restore endogenous Ikaros expression in BCR-ABL1+ B-ALL driven by its knockdown (Ikaros knockdown), and compared these tumors to tumors driven by BCR-ABL1 alone (control). Restoration of Ikaros causes rapid regression of tumor cells in vivo, significantly prolonging tumor transplant recipient survival. Using both transgenic and retroviral approaches, we conducted expression analysis of B-ALL by RNA-Seq and have identified a series of Ikaros-regulated genes within established tumor cell in vivo. Comparison of Ikaros-activated and Ikaros-repressed genes with human B-ALL expression data shows a set of conserved Ikaros target genes, some of which are associated with patient outcome (namely, CTNND1, IFITM3 and EMP1).

2016-12-11 | GSE75976 | GEO

Ikaros-induced gene expression chages upon Ikaros re-expression in the ILC87 Ikaros-deficient tumor cell line

Project description:We used microarrays to analyze gene expression changes in the Ikaros null ILC87 T cell tumor line after re-expression of Ikaros. ILC87 cells were transduced to stably express the 4-hydroxytamoxifen-inducible (4OHT) Ikaros1-ER fusion protein. ILC87-Ik1-ER cells were treated with mock (EtOH) or 4OHT for 1 day and the global gene expression changes were assessed by microarray analysis.

2015-11-03 | E-GEOD-72801 | biostudies-arrayexpress

Mapping of Ikaros and RBPJ binding sites in the mouse T cell leukemia cell line T29

Project description:The transcription factor Ikaros represses Notch signaling. Since Ikaros and Notch treanscriptional mediator RBPJ both recognize sequences that contain the same core TGGGAA motif, it was hypothesized that Ikaros represses Notch signaling by targeting Notch response elements and competing with RBPJ for their binding. Here we used the mouse T-cell leukemia cell line T29 to compare the genomic binding profiles of Ikaros and RBPJ by ChIP-seq. The T29 cell line is derived from a Ikaros-deficient T-cell leukemia (Dumortier et al, MCB 26, 209-220, 2006) and exhibits strong Notch activation. We performed two chip-seq experiments with an anti-RBPJ antibody to map RBPJ binding sites. To map Ikaros binding sites, we engineered a T29-derived cell line that expresses a fusion protein between Ikaros and the ligand binding domain of the estrogen receptor (Ik1-ER) which is activated by addition of 4-hydroxy-tamoxifen (4OHT). We used an anti-Ikaros antibody to map the sites bound by Ik1-ER after treatment of the cells with 4OHT. Sequencing were performed with the Illumina GAII sequencer as as single end 36 base pair reads.

2014-04-02 | E-GEOD-46119 | biostudies-arrayexpress

Genetic analysis of Ikaros target genes and tumor suppressor function in BCR-ABL1<sup>+</sup> pre-B ALL.

Project description:Inactivation of the tumor suppressor gene encoding the transcriptional regulator Ikaros (IKZF1) is a hallmark of BCR-ABL1+ precursor B cell acute lymphoblastic leukemia (pre-B ALL). However, the mechanisms by which Ikaros functions as a tumor suppressor in pre-B ALL remain poorly understood. Here, we analyzed a mouse model of BCR-ABL1+ pre-B ALL together with a new model of inducible expression of wild-type Ikaros in IKZF1 mutant human BCR-ABL1+ pre-B ALL. We performed integrated genome-wide chromatin and expression analyses and identified Ikaros target genes in mouse and human BCR-ABL1+ pre-B ALL, revealing novel conserved gene pathways associated with Ikaros tumor suppressor function. Notably, genetic depletion of different Ikaros targets, including CTNND1 and the early hematopoietic cell surface marker CD34, resulted in reduced leukemic growth. Our results suggest that Ikaros mediates tumor suppressor function by enforcing proper developmental stage-specific expression of multiple genes through chromatin compaction at its target genes.

| S-EPMC5339667 | biostudies-literature

Genome wide mapping of IKAROS binding (ChIP-Seq) in human patient-derived BCR-ABL1+ (Ph+) pre-B ALL xenograft cells

Project description:IKAROS is an important tumor suppressor in human pre-B ALL and is mutated or deleted in a high percentage of human BCR-ABL1+ (Ph+) pre-B ALL. We here report the genome-wide binding of IKAROS in two independent patient-derived BCR-ABL1+ (Ph+) pre-B ALL xenograft cells that express wild type full-length IKAROS.

2017-02-06 | GSE58825 | GEO

Ikaros-regulated microRNA networks in acute lymphoblastic leukemia

Project description:Purpose: miRNAs are important factors that are involved in the regulation cancer growth processes through the regulation of different biological processes. The purpose of the study was to investigate the differential expression pattern of miRNAs in IK1-induced B-ALL cells compared to controls. Methods: In this study, we used two human B-ALL cell lines with IZF1 deletions and induced IK1 expression or controls for 24 hours, and then RNA samples were prepared for the analysis of miRNAs profiles using the Genechip miRNA 4.0 arrays. The Genechip miRNA 4.0 array provides a comprehensive coverage that is designed to interrogate all mature miRNA sequences in miRBase Release 20. Result: The miRNAs expression microarray analysis showed that many miRNAs have been expressed differentially between IK1 and controls. These miRNAs might be involved in the different biological and physiological processes related to growth processes. Conclusion: miRNAs might be an active player Ikaros tumor suppression.

2022-11-17 | GSE209694 | GEO

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