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Analysis of the chromatin accessibility in CPSF6-RARG or NUP98-RARG overexpressing hCD34+ cells compared to control hCD34+ cells using ATAC-seq.

ABSTRACT: Analysis of the chromatin accessibility in CPSF6-RARG or NUP98-RARG overexpressing hCD34+ cells compared to control hCD34+ cells using ATAC-seq.

PROVIDER: PRJNA1150221 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30315581_1.fastq.gz	Fastqsanger.gz
	SRR30315581_2.fastq.gz	Fastqsanger.gz
	SRR30315582_1.fastq.gz	Fastqsanger.gz
	SRR30315582_2.fastq.gz	Fastqsanger.gz
	SRR30315583_1.fastq.gz	Fastqsanger.gz

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Analysis of the chromatin accessibility in CPSF6-RARG or NUP98-RARG overexpressing hCD34+ cells compared to control hCD34+ cells using ATAC-seq.

Project description:We found that RARG fusions selectively upregulated BCL2 and ATF3 in HSPCs, driving uncontrolled proliferation and disrupting the differentiation of RARG-AML cells.To investigate the mechanism how RARG fusions mediate activation of their downstream targets such as BCL2 and ATF3, we defined the chromatin accessibility using ATAC-seq assay in human CD34+ (hCD34+) cells with or without CPSF6::RARG or NUP98::RARG overexpression.

2024-10-16 | GSE275304 | GEO

Identifying RARG fusions or PML-RARA binding genes or analysis the epigenetic changes (H3K27ac, H3K4me1, and H3K4me3) in hCD34+ cells overexpressing CPSF6::RARG and NUP98::RARG.

Project description:To understand how RARG fusion proteins regulate their target genes in the hematopoietic system, we overexpressed fusions or PML-RARA in hCD34+ cells and identified target genes that are regulated by RARG fusions. We found that RARG fusions selectively upregulated BCL2 and ATF3 in HSPCs, driving uncontrolled proliferation and disrupting the differentiation of RARG-AML cells.To investigate the mechanism how RARG fusions mediate activation of their downstream targets such as BCL2 and ATF3, we dected the epigenetic changes (H3K27ac, H3K4me1, and H3K4me3) associated with RARG fusions binding in hCD34+ cells overexpressing CPSF6::RARG and NUP98::RARG.

2024-10-16 | GSE275303 | GEO

The gene expression profiles of leukemia cells isolated from spleens of CreMx-1;CPSF6-RARG mice and Wt1F/+CreMx-1;CPSF6-RARG mice

Project description:We found that CPSF6-RARG fusion gene drives the aberrant expansion of HSCs and progenitor cells, which may lead to a preleukemic phenotype. Moreover, wt1 haploinsufficiency cooperates with RARG fusions to induce AML. To investigate the mechanism by which Wt1 haploinsufficiency cooperates with RARG fusion overexpression to induce AML in vivo, we analyzed the gene expression profiles of leukemia cells isolated from CreMx-1;CPSF6-RARG mice and Wt1F/+CreMx-1;CPSF6-RARG mice through RNA-seq.

2024-10-15 | GSE243415 | GEO

Identifying RARG fusions or PML-RARA binding genes or analysis the epigenetic changes (H3K27ac, H3K4me1, and H3K4me3) in hCD34+ cells overexpressing CPSF6::RARG and NUP98::RARG.

Project description:Identifying RARG fusions or PML-RARA binding genes or analysis the epigenetic changes (H3K27ac, H3K4me1, and H3K4me3) in hCD34+ cells overexpressing CPSF6::RARG and NUP98::RARG.

| PRJNA1150541 | ENA

The effect RARG fusion genes or PML-RARA overexpression in human CD34+ cells on the gene expression.

Project description:Currently, AML with RARG rearrangements (RARG AML), including NUP98-RARG, PML-RARG, CPSF6-RARG, NPM1-RARG, and HNRNPC-RARG, has been identified as a novel entity of AML. Overexpression of RARG fusions in human CD34+ cells promoted the expansion of immature myeloid cells, reduced the percentage of mature granulocytes, inhibited the differentiation of myeloid cells, and self-renewal abilities of hCD34+ cells. To understand how RARG fusion proteins regulate their target genes in the hematopoietic system, we first expressed HA-tagged X-RARG fusions or HA-tagged PML-RARA in hCD34+ cells. We then analyzed the differential genes expression in hCD34+ cells with or without RARG fusion genes or PML-RARA overexpression through RNA-seq.

2024-10-15 | GSE243437 | GEO

The gene expression profiles of leukemia cells isolated from spleens of CreMx-1 CPSF6-RARG mice and Wt1F/+CreMx-1 CPSF6-RARG mice

Project description:The gene expression profiles of leukemia cells isolated from spleens of CreMx-1 CPSF6-RARG mice and Wt1F/+CreMx-1 CPSF6-RARG mice

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transcriptional profiling of NUP98-CDX1, NUP98-CDX4 and EGFP overexpressing primitive mouse bone marrow cells

Project description:The first genetic hits towards leukemia are thought often to confer to the mutant clone a slight proliferative/survial advantage. These pre-malignant clones can then be maintained under physiological cues in normal pool for long periods. We have searched for this type of first genetic hits and found that ectopic expression of novel nucleoporin 98 (NUP98)-homeodomain fusion proteins in primitive bone marrow cells can induce long-lasting hematopoietic stem cell (HSC) activity in these cells. More specifically, NUP98-CDX1/2 was able to sustain HSC activity with high frequencies despite massive in vitro expansions and in vivo residence. Continual expression of NUP98-CDX1/2 did not perturb lymphoid, myeloid or erythroid/platelet differentiation and NUP98-CDX1/2 was able to reprogram committed progenitors into cells with attributes of HSC. Switching off of NUP98-CDX1/2 expression did not lead to “return” to normal HSC but acute differentiation. Related NUP98-CDX4 induced leukemia with the shortest latency ever reported for HOX transcription factors. In this case switching off of NUP98-CDX4 expression cured the full-blown leukemia and again the cured cells showed only transient repopulating activity in vivo. These two types of pre-leukemic cells generated here will provide useful models for elucidating the self-renewal mechanisms of HSC as well as leukemic stem cells. Total RNA from NUP98-CDX lines was compared to EGFP overexpressing lines. The experiment was done in triplicate.

2012-12-01 | E-GEOD-37900 | biostudies-arrayexpress

CPSF6-RARγ Interacts with HDAC3 to Promote Myeloid Transformation [CUT&Tag in CD34+ cells]

Project description:Acute myeloid leukemia (AML) with RARG fusions, which clinic features resemble acute promyelocytic leukemia (APL), have been identified as a new subtype with poor clinical outcomes. The underlying mechanism of RARG fusion is poorly understood, which needs to be explored urgently to develop effective therapeutic strategies. Using hematopoietic specific knock-in mouse model and xenograft mouse model transplanted with oncogene transduced human CD34+ cells, we revealed that CPSF6-RARG (CR) fusion, one of the most prevalent recurrent RARG translocations, enhances expansion of immature cells and impairs myeloid maturation, synergizing with RAS mutation to drive more aggressive myeloid malignancies. Mechanistically, CR recruits the histone deacetylase 3 (HDAC3) to suppress the transcription of PU.1, a key transcription factor for myeloid lineage specification. CR driven leukemia is more sensitive to HDAC inhibitors in vitro and in vivo. Hence, our data reveals the molecular bases of the oncogenic CR fusion and provides a potential targeted therapeutic approach against AML with CR fusions.

2024-10-24 | GSE245012 | GEO

CPSF6-RARγ Interacts with HDAC3 to Promote Myeloid Transformation [RNA-seq]

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CPSF6-RARγ Interacts with HDAC3 to Promote Myeloid Transformation [BM Mac1+ and c-kit+ cells RNA-seq]

2024-10-24 | GSE245028 | GEO