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

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

PROVIDER: PRJNA752579 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15359324_1.fastq.gz	Fastqsanger.gz
	SRR15359324_2.fastq.gz	Fastqsanger.gz
	SRR15359325_1.fastq.gz	Fastqsanger.gz
	SRR15359325_2.fastq.gz	Fastqsanger.gz
	SRR15359326_1.fastq.gz	Fastqsanger.gz

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The megakaryocytic transcription factor ARID3A suppresses leukemia pathogenesis.

Project description:The megakaryocytic transcription factor ARID3A suppresses leukemia pathogenesis.

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

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

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

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

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

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

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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

CMK LC-MS/MS after CoIP of ARID3A

Project description:In order to determine proteins interacting with ARID3A in the ML-DS cell line CMK, we performed CoIP of endogenous ARID3A followed by LC-MS/MS

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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

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