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NUP98-HOXA9 acute myeloid leukemia

ABSTRACT: Mass Spectrometry analysis of the interactome of the oncoprotein NUP98-HOXA9

INSTRUMENT(S): LTQ Orbitrap Velos

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture, Early Embryonic Cell

DISEASE(S): Acute Leukemia

SUBMITTER: Fernando Garcia

LAB HEAD: Javier Muñoz

PROVIDER: PXD001828 | Pride | 2017-07-10

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	20130626_FG_Cigudosa_EV_BIO1_01-01.pep.xml	Pepxml
	20130626_FG_Cigudosa_EV_BIO1_01.raw	Raw
	20130626_FG_Cigudosa_EV_BIO2_01-01.pep.xml	Pepxml
	20130626_FG_Cigudosa_EV_BIO2_01.raw	Raw
	20130626_FG_Cigudosa_H_BIO1_01-01.pep.xml	Pepxml

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Publications

The molecular pathogenesis of the NUP98-HOXA9 fusion protein in acute myeloid leukemia.

Rio-Machin A A Gómez-López G G Muñoz J J Garcia-Martinez F F Maiques-Diaz A A Alvarez S S Salgado R N RN Shrestha M M Torres-Ruiz R R Haferlach C C Larráyoz M J MJ Calasanz M J MJ Fitzgibbon J J Cigudosa J C JC

Leukemia 20170620 9

PMID: 28630438

Similar Datasets

MLL is essential for NUP98-HOXA9-induced leukemia

Project description:Rearrangements involving the NUP98 gene resulting in fusions to several partner genes occur in acute myeloid leukemia and myelodysplastic syndromes. This study demonstrates that the second FG repeat domain of the NUP98 moiety of the NUP98-HOXA9 fusion protein is important for its cell immortalization and leukemogenesis activities. We demonstrate that NUP98-HOXA9 interacts with MLL via this FG repeat domain and that, in the absence of MLL, NUP98-HOXA9-induced cell immortalization and leukemogenesis are severely inhibited. Molecular analyses indicate that MLL is important for the recruitment of NUP98-HOXA9 to the HOXA locus and for NUP98-HOXA9-induced HOXA gene expression. Our data indicate that MLL is crucial for NUP98-HOXA9 leukemia initiation.

2017-02-28 | GSE93923 | GEO

Transcription profiling of mouse bone marrow cells expressing NUP98/HHEX or NUP98/HOXA9 a new oncogenic fusion with acute myeloid leukemia

Project description:We have cloned and characterized a fusion gene NUP98/HHEX1 resulting from t(7;10) from a patient with acute myeloid leukemia (AML). As NUP98/HHEX acts as an aberrant transcriptional activator, putative targets were searched upon transient expression of the fusion in primary murine bone marrow cells. Experiment Overall Design: Murine bone marrow cells were transduced with a retrovirus (MSCV-IRES-GFP, MIG) expressing either NUP98/HHEX or NUP98/HOXA9 (or the empty vector), mRNA was isolated after 72h. Each experiment was performed in triplicates.

2008-06-11 | E-GEOD-10909 | biostudies-arrayexpress

Hoxa9 and Meis1 cooperatively induce addiction to Syk signaling by suppressing miR-146a in acute myeloid leukemia

Project description:The transcription factor Meis1 drives myeloid leukemogenesis in the context of Hox gene overexpression but is currently considered undruggable. We therefore investigated whether myeloid progenitor cells transformed by Hoxa9 and Meis1 become addicted to targetable signaling pathways. A comprehensive (phospho)proteomic analysis revealed that Meis1 increased Syk protein expression and activity. Syk upregulation occurs through a Meis1-dependent feed-forward loop. By dissecting this loop, we show that Syk is a direct target of miR-146a, whose expression is indirectly regulated by Meis1 through the transcription factor PU.1. In the context of Hoxa9 overexpression, Syk induces Meis1, recapitulating several leukemogenic features of Hoxa9/Meis1-driven leukemia. Finally, we show that Syk inhibition disrupts the identified regulatory loop, prolonging survival of mice with Hoxa9/Meis1-driven leukemia.

2017-06-14 | PXD004192 | Pride

Evaluation of the NUP98-HOXA9 role as oncogenic transcription factor

Project description:To study the oncogenic mechanism triggered by the leukemic fusion protein NUP98-HOXA9, we cloned the cDNA of NUP98-HOXA9 into a retroviral vector (pMSCV-IRES-GFP) and efficiently transduced the HEK293FT human cell line. We performed a ChIP-seq analysis to identify the DNA binding sites of NUP98-HOXA9. These results allowed us to demonstrate that NUP98-HOXA9 regulates the expression of genes involved in the development of Acute Myeloid Leukemia by directly interacting with their enhancer regions. We further investigated the functional contribution to the DNA binding profile of the two moieties that compose the fusion protein. We cloned the coding region of HOXA9 wt and NUP98 wt in the same retroviral vector, established two new cellular models, 293FT-HOXA9 and 293FT-NUP98, and performed separate ChIP-seq analyses. We demonstrated that both moieties contribute importantly to the regulation of the target genes.

2016-12-31 | GSE62586 | GEO

Gene expression profiling of NUP98-HOXA9 expressing mouse embryonic stem cells

Project description:To investigate the effect of NUP98-HOXA9 on global gene expression, we established FLAG-NUP98-HOXA9 expressing mouse embryonic stem cell lines.

2023-07-25 | GSE227199 | GEO

The role of Hoxa9 and Meis1 in development of acute myeloid leukemia (mRNA)

Project description:OBJECTIVE: MEIS1, a HOX cofactor, collaborates with multiple HOX proteins, such as HOXA9, to accelerate the onset of acute myeloid leukemia (AML) through largely unknown molecular mechanisms. To further resolve these mechanisms, we conducted a structure-function analysis of Meis1 and gene expression profiling, in the context of Hoxa9 leukemogenesis. RESULTS: We show, in a murine bone marrow transplantation model, that the homeodomain of Meis1 is required for leukemogenic collaboration with Hoxa9. Gene expression profiling of a Hoxa9 preleukemic cell line transduced with wild-type or Meis1 homeodomain mutant reveal deregulation of multiple genes including a set not previously implicated as Meis1 targets. Murine bone marrow cells transduced with Hoxa9-GFP + empty MIY vector were compared to Hoxa9+Meis1 cells or Hoxa9+Meis1 with deleted homeodomain (DHD) cells and cultured for three or four weeks before harvest for miRNA expression array. Four independent experiments were performed for each of the three different conditions included in the study. Cells from all samples were also transplanted into lethally irradiated mice to test for their transforming and leukemic potential.

2016-09-01 | E-GEOD-75272 | biostudies-arrayexpress

The role of Hoxa9 and Meis1 in development of acute myeloid leukemia

2017-04-27 | GSE74566 | GEO

The role of Hoxa9 and Meis1 in development of acute myeloid leukemia (mRNA)

2016-09-01 | GSE75272 | GEO

Development of NUP98-HOXA9 gene expression signatures

Project description:To explore the molecular mechanisms induced by the leukemic fusion protein NUP98-HOXA9, we performed gene expression analysis of human hematopoietic progenitors and primary samples of patients that express NUP98-HOXA9. By combining these data with ChIP-seq results, we observed that the fusion protein is able to both activate and repress the expression of its target genes.

2016-12-31 | GSE62585 | GEO

Expression data from murine hematopoietic cells expressing BCR-ABL alone, NUP98-HOXA9 alone, BCR-ABL and NUP98-HOXA9, or null for both oncogenes

Project description:Leukemia is a complex malignancy with hundreds of distinct mutations associated with disease development. Studies have shown that oncogenes cooperate to promote leukemia transformation, however, the downstream effectors of this cooperation are largely unknown. Using a genetically defined mouse model of acute leuekmia, we investigated the regulated of genes downstream of the cooperative oncogenic interaction between BCR-ABL and NUP98-HOXA9 and identified a unique gene signature abberrantly expression in leukemia. Total RNA was isolated from hematopoietic cells transduced with BCR-ABL and Nup98-HOXA9 retroviruses and transplanted into recipient mice. Bone marrow cells were purified by GFP (BCR-ABL) and YFP (NUP98-HOXA9) using FACS.

2012-05-10 | E-GEOD-37907 | biostudies-arrayexpress

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