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Gene expression changes after loss of Hoxa9 in transformed HSCs [HOXA9 RNA-seq]

ABSTRACT: Characterization of gene expression changes 72 hours after withdrawal of tamoxifen in murine hematopoietic progenitors transformed by Hoxa9-ER/Meis1 using RNAseq. In the presence of tamoxifen (4OHT), Hoxa9-ER localizes to the nucleus of cells allowing for transformation, while withdrawal of 4OHT (culture in EtOH) leads to loss of nuclear Hoxa9-ER. Loss of Hoxa9-ER leads to a decrease in cellular proliferation and differentiation along the myeloid lineage.

ORGANISM(S): Mus musculus

PROVIDER: GSE58359 | GEO | 2014/06/11

SECONDARY ACCESSION(S): PRJNA252110

REPOSITORIES: GEO

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Gene expression changes after loss of Hoxa9 in transformed HSCs [HOXA9 RNA-seq]

Project description:Characterization of gene expression changes 72 hours after withdrawal of tamoxifen in murine hematopoietic progenitors transformed by Hoxa9-ER/Meis1 using RNAseq. In the presence of tamoxifen (4OHT), Hoxa9-ER localizes to the nucleus of cells allowing for transformation, while withdrawal of 4OHT (culture in EtOH) leads to loss of nuclear Hoxa9-ER. Loss of Hoxa9-ER leads to a decrease in cellular proliferation and differentiation along the myeloid lineage. Examination of gene expression by RNAseq in two conditions in biological replicates.

2014-06-11 | E-GEOD-58359 | biostudies-arrayexpress

Gene expression changes after loss of C/EBPα in transformed HSCs [CEBPA RNA-seq]

Project description:RNAseq characterization of gene expression changes 72 hours after genomic excision of Cebpa in murine hematopoietic progenitors from Cebpaf/f;CreER mice transformed by Hoxa9/Meis1. In the presence of tamoxifen (4OHT), Cre-ER localizes to the nucleus of cells allowing for excision of Cebpa and loss of C/EBPα protein levels. Loss of C/EBPα leads to a decrease in cellular proliferation.

2014-06-11 | GSE58360 | GEO

Gene expression changes after loss of C/EBPα in transformed HSCs [CEBPA RNA-seq]

2014-06-11 | E-GEOD-58360 | biostudies-arrayexpress

Genome-wide co-occupancy of Hoxa9 and C/EBPα in Hoxa9/Meis1 transformed HSCs [ChIP-seq]

Project description:Identification of the genome-wide binding sites of Hoxa9 and C/EBPα in a murine myeloblastic cell line transformed by Hoxa9/Meis1. Over 50% of Hoxa9 binding sites are co-bound by C/EBPα, providing mechanistic insight into the requirement of C/EBPα for Hoxa9-mediated leukemogenesis. Additionally, genome-wide occupancy of H3K4 monomethylation and H3K27 trimethylation provide additional information on the functionality of Hoxa9/C/EBPα cobound loci.

2014-06-11 | GSE58361 | GEO

Genome-wide co-occupancy of Hoxa9 and C/EBPα in Hoxa9/Meis1 transformed HSCs [ChIP-seq]

2014-06-11 | E-GEOD-58361 | 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

ChIP-seq of the HOXA9 and MEIS1 transcription factors in SEM cells.

Project description:SEM cells were established from the peripheral blood of a 5-year-old girl in relapse with acute lymphoblastic leukaemia (ALL). SEM cells exhibit the t(4;11) chromosomal rearrangement, which leads to production of the MLL-AF4 fusion protein. Hematopoietic transcription factors including HOXA9 and MEIS1 are highly expressed in ALL. ChIP-seq was performed against HoxA9 and MEIS1 in SEM cells. DNA was enriched by chromatin immunoprecipitation (ChIP) and analyzed by Solexa sequencing.

2012-05-31 | E-GEOD-38339 | biostudies-arrayexpress

Gene expression profiles upon Meis1 knockout in Hoxa9/Meis1-induced AML

Project description:Meis1 is found cooperatively activated with Hoxa7/a9 in AML, and it indeed promotes leukemogenic activities of Hoxa9. It is important to identify downstream target genes of Meis1 to understand its cooperative activity with Hoxa9 in leukemogenesis. We used microarrays to detail the global programme of gene expression upon Meis1 knockout. Murine primary bone marrow cells of the Rosa26-Cre-ERT2 knock-in mouse were transformed by retroviral transduction of Hoxa9 and floxed Meis1. The immortalized bone marrow cells were treated with 2 μM of 4-hydroxytamoxifen to delete Meis1 cDNA. Gene expression profiles were compared between the original Hoxa9/Meis1-expressing cells and Meis1 deleted (Hoxa9 only) cells.

2015-01-01 | E-GEOD-50645 | biostudies-arrayexpress

Effect of loss of Jmjd1c on Hoxa9/Meis1 leukemia

Project description:Analysis of gene expression profile of Hoxa9/Meis1 leukemia cells 6 days after loss of Jmjd1c. Loss of Jmjd1c induces differentiation and Hoxa9/Meis1 leukemia cells. These results provide insight into the role of Jmjd1c in AML with elelvated expression of Hoxa9.

2016-06-09 | GSE75580 | GEO

RNAseq of murine primary bone marrow cells transformed by an inducible Hoxa9-ER: time-course

Project description:Relative overexpression of HOXA9 is a key feature of aggressive AML (acute myeloid leukemia). Hoxa9 responsive genes were identified by nascent RNA sequencing (4-thio-uridine labeled RNA - sequencing) in samples of primary hematopoietic precursor cells from mice transformed by an tamoxifen inducible version of Hoxa9 (Hoxa9-ER). Samples were generated in the presence of active Hoxa9 (0h) and in a time series after Hoxa9 was inactivated at 8h, 16h, 24h, 48h, and 72h.

2019-04-13 | E-MTAB-7107 | biostudies-arrayexpress

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