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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE38339 | GEO | 2012/05/31

SECONDARY ACCESSION(S): PRJNA167740

REPOSITORIES: GEO

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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

Genes differentially expressed in MLL-AF9-transduced versus HOXA9/MEIS1-transduced LSK cells

Project description:HOXA9 and MEIS1 are essential downstream effectors of the MLL-AF9 oncoprotein during leukaemia induction. Leukaemia derived from MLL-AF9-transduced LSK cells has a more aggressive phenotype than that derived from HOXA9/MEIS1-transduced LSK cells. To determine differential gene expression that contributes to increased aggressiveness in MLL-AF9-induced leukaemia, microarray was performed on LSK cells transduced with MLL-AF9 versus HOXA/MEIS1 oncogenes.

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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.

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

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RNA expression changes in HOXA9/MEIS1 leukemia cells

Project description:Aberrant expression of homeobox transcription factor HOXA9 is a central component of the leukemogenic program driven by diverse oncogenes. Here we show that HOXA9 overexpression in myeloid progenitor cells and pro-B cells leads to significant rearrangement of the epigenetic landscape with prominent emergence of cancer specific de novo enhancers. HOXA9 acts as a pioneer factor at the de novo enhancers and is required for recruitment of transcription factor CEBP/a and the histone H3K4 methyltransferase MLL3/MLL4 complex. HOXA9 function at the de novo enhancer is distinct from its physiological role at distal enhancers during normal hematopoietic development. Genetic deletion of MLL3/4 specifically affects the active enhancer signatures at de novo enhancers and inhibits HOXA9/MEIS1-mediated leukemogenesis. Our study reveals a previously uncharacterized role of HOXA9 and the MLL3/4 complex in leukemogenesis and provide mechanistic insights in epigenetic deregulation during malignant transformation.

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Effect of loss of Jmjd1c on Hoxa9/Meis1 leukemia

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Chromatin state changes in HOXA9/MEIS1 leukemia cells [ChIP-Seq]

Project description:Aberrant expression of homeobox transcription factor HOXA9 is a central component of the leukemogenic program driven by diverse oncogenes. Here we show that HOXA9 overexpression in myeloid progenitor cells and pro-B cells leads to significant rearrangement of the epigenetic landscape with prominent emergence of cancer-specific de novo enhancers. HOXA9 acts as a pioneer factor at the de novo enhancers and is required for recruitment of transcription factor CEBP/ and the histone H3K4 methyltransferase MLL3/MLL4 complex. The HOXA9 function at de novo enhancers is distinct from its physiological role at enhancers during normal hematopoietic development. The MLL3/MLL4 complex physically interacts with HOXA9 and is required both for the active enhancer signatures at de novo enhancers and HOXA9/MEIS1-mediated leukemogenesis. The findings suggest that therapeutic targeting of HOXA9-dependent histone methylation could be an effective therapeutic strategy in acute leukemia associated with HOXA9 over expression.

2018-09-05 | GSE103446 | GEO

Chromatin state changes in HOXA9/MEIS1 leukemia cells [4C-Seq]

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MLL-rearranged acute lymphoblastic leukemias upregulate BCL-2 through H3K79 methylation and are highly sensitive to the BCL-2 specific antagonist ABT-199

Project description:We present ChIP-seq in the t(4;11) cell line SEM for different components of the MLL-AF4 complex as well as other chromatin proteins Examination of 5 histone marks, MLL, AF4, ENL and CFP1 in t(4;11) cells

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