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The megakaryocytic transcription factor ARID3A suppresses leukemia pathogenesis.

ABSTRACT: The megakaryocytic transcription factor ARID3A suppresses leukemia pathogenesis.

PROVIDER: PRJNA752569 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15359318_1.fastq.gz	Fastqsanger.gz
	SRR15359318_2.fastq.gz	Fastqsanger.gz
	SRR15359319_1.fastq.gz	Fastqsanger.gz
	SRR15359319_2.fastq.gz	Fastqsanger.gz
	SRR15359320_1.fastq.gz	Fastqsanger.gz

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The megakaryocytic transcription factor ARID3A suppresses leukemia pathogenesis [CUT&RUN]

Project description:The megakaryocytic transcription factor ARID3A suppresses leukemia pathogenesis [CUT&RUN]

| PRJNA752579 | ENA

The megakaryocytic transcription factor ARID3A suppresses leukemia pathogenesis [ATAC-seq]

Project description:The megakaryocytic transcription factor ARID3A suppresses leukemia pathogenesis [ATAC-seq]

| PRJNA752582 | ENA

The megakaryocytic transcription factor ARID3A suppresses leukemia pathogenesis [RNA-seq]

Project description:The megakaryocytic transcription factor ARID3A suppresses leukemia pathogenesis [RNA-seq]

| PRJNA752580 | ENA

The megakaryocytic transcription factor ARID3A suppresses leukemia pathogenesis [ATAC-seq]

Project description:The purpose of this study was to decipher the molecular function of ARID3A. We leveraged gene expression (RNA-Seq) and chromatin profiling (ATAC-Seq and CUT&RUN) to evaluate gene expression changes upon restoring Arid3a expression in the context of the Gata1s mutation and miR-125b overexpression

2022-04-20 | GSE181569 | GEO

The megakaryocytic transcription factor ARID3A suppresses leukemia pathogenesis [CUT&RUN]

2022-04-20 | GSE181568 | GEO

The megakaryocytic transcription factor ARID3A suppresses leukemia pathogenesis [RNA-seq]

2022-04-20 | GSE181567 | GEO

The megakaryocytic transcription factor ARID3A suppresses leukemia pathogenesis.

Project description:Given the plasticity of hematopoietic stem and progenitor cells, multiple routes of differentiation must be blocked in the the pathogenesis of acute myeloid leukemia, the molecular basis of which is incompletely understood. We report that posttranscriptional repression of the transcription factor ARID3A by miR-125b is a key event in the pathogenesis of acute megakaryoblastic leukemia (AMKL). AMKL is frequently associated with trisomy 21 and GATA1 mutations (GATA1s), and children with Down syndrome are at a high risk of developing the disease. The results of our study showed that chromosome 21-encoded miR-125b synergizes with Gata1s to drive leukemogenesis in this context. Leveraging forward and reverse genetics, we uncovered Arid3a as the main miR-125b target behind this synergy. We demonstrated that, during normal hematopoiesis, this transcription factor promotes megakaryocytic differentiation in concert with GATA1 and mediates TGFβ-induced apoptosis and cell cycle arrest in complex with SMAD2/3. Although Gata1s mutations perturb erythroid differentiation and induce hyperproliferation of megakaryocytic progenitors, intact ARID3A expression assures their megakaryocytic differentiation and growth restriction. Upon knockdown, these tumor suppressive functions are revoked, causing a blockade of dual megakaryocytic/erythroid differentiation and subsequently of AMKL. Inversely, restoring ARID3A expression relieves the arrest of megakaryocytic differentiation in AMKL patient-derived xenografts. This work illustrates how mutations in lineage-determining transcription factors and perturbation of posttranscriptional gene regulation can interact to block multiple routes of hematopoietic differentiation and cause leukemia. In AMKL, surmounting this differentiation blockade through restoration of the tumor suppressor ARID3A represents a promising strategy for treating this lethal pediatric disease.

| S-EPMC9632760 | biostudies-literature

The megakaryocytic transcription factor ARID3A suppresses leukemia pathogenesis.

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

2022-04-20 | GSE181570 | GEO

Chromosome 21-encoded miR-125b cooperates with GATA1s in trisomy 21-associated megakaryoblastic leukemia by targeting the megakaryocytic transcription factor ARID3A III

Project description:The purpose of this study was to decipher the gene expression changes in the ML-DS cell line CMK upon overexpression of ARID3A. For that, we used a doxycycline-inducible gene expression system to overexpress ARID3A

2022-04-20 | GSE169740 | GEO

SON inhibits megakaryocytic differentiation via repressing the megakaryocytic gene expression program in acute megakaryoblastic leukemia

Project description:A high incidence of acute megakaryoblastic leukemia (AMKL) in Down syndrome patients implies that chromosome 21 genes have a pivotal role in AMKL development, but the functional contribution of individual genes remains elusive. Here, we report that SON, a chromosome 21-encoded DNA- and RNA-binding protein, inhibits megakaryocytic differentiation by suppressing RUNX1 and the megakaryocytic gene expression program. As megakaryocytic progenitors differentiate, SON expression is drastically reduced, with mature megakaryocytes having the lowest levels. In contrast, AMKL cells express an aberrantly high level of SON, and knockdown of SON induced the onset of megakaryocytic differentiation in AMKL cell lines. Genome-wide transcriptome analyses revealed that SON knockdown turns on the expression of pro-megakaryocytic genes while reducing erythroid gene expression. Mechanistically, SON represses RUNX1 expression by directly binding to the proximal promoter and two enhancer regions, the known +23 kb enhancer and the novel +139 kb enhancer, at the RUNX1 locus to suppress H3K4 methylation. In addition, SON represses the expression of the AP-1 complex subunits JUN, JUNB and FOSB which are required for late megakaryocytic gene expression. Our findings define SON as a negative regulator of RUNX1 and megakaryocytic differentiation, implicating SON overexpression in impaired differentiation during AMKL development.

2020-09-01 | GSE157178 | GEO

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