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Gata2 promotes drug resistance in Acute Myeloid Leukemia (AML) [ChIP-Seq]

ABSTRACT: In this study, we generated mouse models of MLL-AF9-driven AML (MA9) harboring conditional alleles for Gata2 gene to precisely investigate the role of Gata2 in drug resistance and progression of MLL-rearranged (MLL-r) AML. Our findings revealed a novel mechanism for Gata2 in blunting p53 mediated apoptosis via transcriptional repression of Rassf4, a regulator of Mdm2 protein stability.

ORGANISM(S): Mus musculus

PROVIDER: GSE264719 | GEO | 2025/04/30

REPOSITORIES: GEO

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Gata2 promotes drug resistance in Acute Myeloid Leukemia (AML)

Project description:In this study, we generated mouse models of MLL-AF9-driven AML (MA9) harboring conditional alleles for Gata2 gene to precisely investigate the role of Gata2 in drug resistance and progression of MLL-rearranged (MLL-r) AML. Our findings revealed a novel mechanism for Gata2 in blunting p53 mediated apoptosis via transcriptional repression of Rassf4, a regulator of Mdm2 protein stability.

2025-05-01 | GSE266623 | GEO

RNA profiling of Suv39h1 overexpressed MLL-AF9 induced acute myeloid leukemia (AML) cells

Project description:Acute myeloid leukemias (AMLs) with rearrangement of the mixed-lineage leukemia (MLL) gene are the most aggressive hematopoietic malignancies. By analyzing the clinical data, we found the expression of SUV39H1 was significantly decreased in AML patients and MLL-AF9 (MA9) induced AML mice, in comparison with controls. Remarkably, when overexpress Suv39h1 in MA9 AML mice, the survival of AML mice was significantly prolonged.To examined the mechanism mediated by Suv39h1 overexpression (SUV-OE), we performed the RNAseq profiling of SUV-OE MA9 AML cells and control cells.

2020-12-22 | GSE115549 | GEO

Fabp4 is Essential for the Maintenance of Leukemia Stem Cells while Sparing Hematopoietic Stem Cells

Project description:Fatty acid-binding protein 4 (FABP4) plays a crucial role in the uptake, transport, and metabolic regulation of fatty acids. Previous research has found that the abnormal expression of FABP4 is associated with certain cancers, and it may become a new target for tumor therapy. We discovered that a haploinsufficient or absent dosage of Fabp4 does not affect the function of hematopoietic stem cells in mice, but significantly impacts the maintenance of leukemia stem cells (LSC). Our findings indicate that while Fabp4 does not influence the initiation of acute myeloid leukemia (AML) transformed by MLL-AF9 (MA9) in mice, it markedly promotes the progression of AML. A haploinsufficient or absent dosage of Fabp4 significantly extends the survival time of MA9 mice. Our research reveals the key role and mechanism of Fabp4 in MA9-LSC, suggesting that Fabp4 is a potential target for selectively eliminating MLL-rearranged leukemia.

2025-03-23 | GSE278587 | GEO

Fabp4 is Essential for the Maintenance of Leukemia Stem Cells while Sparing Hematopoietic Stem Cells [bulkRNA-seq]

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RNA sequencing expression analysis of murine MLL-AF9;NRAS acute myeloid leukemia cells silenced for E2-2.

2016-06-29 | GSE80745 | GEO

Integrative epigenomic analysis in MLL-AF9 acute myeloid leukemia (AML) and B-acute lymphoblastic leukemia (B-ALL)

Project description:Next generation DNA sequencing of acute myeloid leukemia (AML) patient samples has revealed novel recurrent mutations while at the same time highlighting the genetic heterogeneity of the disease. These observations suggest that an extraordinarily large number of combinations of mutations can contribute to leukemogenesis. In order to address the question of the contribution of patient genetic background to AML we have developed a model system to generate multiple human leukemias in a single donorâs genetic background. Stepwise RNA-seq data from this model shows that in the context of AML driven by the MLL-AF9 (MA9) oncogene, the genetic background of the donor does not have a detectable effect. Comparison of these model leukemias from multiple single donors to AML patient samples containing MA9 translocations revealed conserved gene expression patterns not previously highlighted in this genetic sub-type. We further demonstrate that the expression of one of these genes, RET, is essential both in vivo and in vitro growth of MA9 AMLs . study of methylome during the development of MLL-AF9 AML

2017-05-02 | E-GEOD-70755 | biostudies-arrayexpress

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2017-05-02 | E-GEOD-72061 | biostudies-arrayexpress

RNA sequencing expression analysis of murine MLL-AF9;NRAS acute myeloid leukemia cells silenced for E2-2.

Project description:We investigated the role of the transcriptional regulators Id2 and E2-2 (encoded by Tcf4) in the context of MLL-rearranged acute myeloid leukemia (AML). Using an AML mouse model driven by a Tet-off inducible MLL-AF9 allele co-expressed with oncogenic NRASG12D, we demonstrated that MLL-AF9 regulates the E protein pathway by suppressing Id2, while activating the expression of its target E2-2. Moreover, we found that Id2 over-expression in MLL-AF9 AML cells results inhibition of leukemia growth, loss of leukemia stem cell-associated gene expression pattern and induction of differentiation. E2-2 silencing phenocopies Id2 overexpression in MLL-AF9-AML cells. To study the gene expression changes associated with E2-2 depletion in the context of MLL-rearranged AML, RNA sequencing analysis was performed on MLL-AF9;NRAS AML cells transduced with vectors expressing hairpins against E2-2 (shTcf4#654 and shTcf4#3646) or a control hairpin against Renilla luciferase (shRen). Primary AMLs driven by MLL/AF9 expression linked to cherry reporter, in association with oncogenic NRASG12D (MLL/AF9;NRAS) were generated by reconstituting lethally irradiated congenic mice with fetal liver cells co-transduced with the MSCV-MLL/AF9-IRES-cherry retroviral vector and a second vector co-expressing NRASG12D together with luciferase (MSCV-luciferase-IRES-NRASG12D). RNA sequencing analysis sequencing analysis was performed on MLL-AF9;NRAS AML cells transduced in vitro with vectors expressing hairpins against E2-2 (shTcf4#654 and shTcf4#3646) or a control hairpin against Renilla luciferase (shRen) linked to the reporter GFP. Viable GFP-positive cells were FACS-sorted 2 days after transduction and used for RNA sequencing analysis. Two independent biological replicates of the experiment were used for the RNA sequencing (9-5-14 and 14-4-14).

2016-06-29 | E-GEOD-80745 | biostudies-arrayexpress

RNA-seq of murine MA9 Gata2 f/f and Gata2 -/- (Gata2 KO) leukemias.

Project description:Transcriptional effects of Gata2 deletion in murine MA9 leukemia.

2025-04-30 | GSE265756 | GEO

Zinc finger protein 521 overexpression is a feature of MLL-rearranged acute myeloid leukemia and contributes to the maintenance of myeloid differentiation block

Project description:ZNF521 is a multiple zinc finger transcription factor previously identified because abundantly and selectively expressed in normal CD34+ hematopoietic stem and progenitor cells. From microarray datasets, aberrant expression of ZNF521 has been reported in both pediatric and adult acute myeloid leukemia (AML) patients with MLL gene rearrangements. However, a proper validation of microarray data is lacking, likewise ZNF521 contribution in MLL-rearranged AML is still uncertain. In this study, we show that ZNF521 is significantly upregulated in MLL translocated AML patients from a large pediatric cohort, regardless of the type of MLL translocations such as MLL-AF9, MLL-ENL, MLL-AF10 and MLL-AF6 fusion genes. Our in vitro functional studies demonstrate that ZNF521 play a critical role in the maintenance of the undifferentiated state of MLL-rearranged cells. Furthermore, analysis of the ZNF521 gene promoter region shows that ZNF521 is a direct downstream target of both MLL-AF9 and MLL-ENL fusion proteins. Gene expression profiling of MLL-AF9-rearranged THP-1 cells after depletion of ZNF521 reveals correlation with several expression signatures including stem cell-like and MLL fusion dependent programs. These data suggest that MLL fusion proteins activate ZNF521 expression to maintain the undifferentiated state and contribute to leukemogenesis. ZNF521 is required to block differentiation in MLL-rearranged AML cells

2017-03-31 | GSE79110 | GEO

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