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Twist family BHLH transcription factor 1 is required for the maintenance of leukemia stem cell in MLL-AF9+ acute myeloid leukemia

ABSTRACT: To identify the downstream targets of TWIST1 or Hoxa9, we carried out RNA sequencing to characterize transcriptional changes upon Twist1 deletion or Hoxa9 knockdown in LSCs from MLL-AF9+ AML mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE215026 | GEO | 2025/10/06

REPOSITORIES: GEO

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A liquid chromatography-tandem mass spectrometry analysis of endogenous TWIST1 immunoprecipitates in the LSCs from MLL-AF9+ AML mice

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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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Project description:How the stemness of adult stem cells and cancer stem cells is regulated by environmental cues through surface receptors is poorly understood. In this gene expression analysis, we found that, in the mouse MLL-AF9 acute myeloid leukemia (AML) model, a deficiency in intracellular signaling of inhibitory receptor PIR-B resulted in increased differentiation and decreased stemness of leukemia stem cells, revealing that PIR-B supports leukemia development. Our study indicates unexpected functional significance of a classical immune inhibitory receptor in the maintenance of stemness of cancer stem cells. Total RNA obtained from wild-type MLL-AF9 LSCs compared to PirBTM MLL-AF9 LSCs

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Differential accessibility landscapes in MLL-AF9-driven leukemia stem cells upon inhibiiton of purine metabolism

Project description:Targeted metabolomics analysis of bulk leukemia cells and leukemia stem cells (LSCs) derived from the MLL-AF9-driven acute myeloid leukemia (AML) model, and normal granulocyte-monocyte progenitor (GMP) cells and whole bone marrow (WBM) cells from healthy mice, revealed an enhanced purine metabolism in AML LSCs. Inhibiting the purine biosynthetic pathway using mycophenolate mofetil (MMF) promoted myeloid differentiation and induced alterations in the chromatin accessibility landscape. These findings underscore the pivotal role of purine metabolism in regulating LSC activity.

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Effect of sgRNA-mediated disruption of GLUT1 on gene expression on c-Kit+ MLL::AF9 leukemia cells

Project description:Acute myeloid leukemia (AML) is initiated and propagated by leukemia stem cells (LSCs), a self-renewing population of leukemia cells. Here we performed an in vivo CRISPR screen and identified the facilitated glucose transporter type 1 (GLUT1) as a critical metabolic dependency for murine MLL::AF9 LSCs. GLUT1 disruption by genetic ablation or by pharmacological inhibition with BAY-876 led to suppression of leukemia progression and improved survival in an MLL::AF9 mouse model of AML. Glut1 inhibition further resulted in glycolytic suppression, decreased levels of tricarboxylic cycle intermediates, and elevated levels of amino acids. These changes in metabolic profile coincided with increased autophagic activity and differentiation of AML cells. Notably, dual inhibition of GLUT1 and oxidative phosphorylation exhibited synergistic anti-leukemic effects in human AML cells. Collectively, these findings increase our understanding of how murine LSCs are metabolically regulated and highlight GLUT1 inhibition as a promising therapeutic adjuvant approach in AML.

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Project description:To investigate whether co-expression of PBX3/MEIS1 can mimic that of MLL-AF9, HOXA9/MEIS1 or HOXA9/PBX3 in inducing leukemogenesis, we conducted in vivo mouse bone marrow transplantation (BMT) assays. Briefly, normal mouse bone marrow (BM) progenitor (i.e., lineage negative; Lin-) cells collected from B6.SJL (CD45.1) donor mice (CD45.1) were retrovirally co-transduced with MSCVneo-MLL-AF9+MSCV-PIG (MLL-AF9), MSCVneo-HOXA9+MSCV-PIG (HOXA9), MSCVneo-HOXA9+MSCV-PIG-MEIS1 (HOXA9+MEIS1), MSCVneo-HOXA9+MSCV-PIG-PBX3 (HOXA9+PBX3), MSCV-PIG-PBX3+MSCVneo-MEIS1 (PBX3+MEIS1), MSCVneo+MSCV-PIG-PBX3 (PBX3) , MSCVneo+MSCV-PIG-MEIS1 (MEIS1), or MSCVneo+MSCV-PIG (normal control; NC). Retrovirally transduced cells then were cultured with cytokines as well as puromycin and G418. Seven days later, the donor cells were transplanted into lethally irradiated (960 rads) 8- to 10-week-old C57BL/6 (CD45.2) recipient mice. The transplanted mice were watched for leukemogenesis. Then, gene expression profiling was conducted with bone marrow samples collected from leukemia groups and control group.

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Twist family BHLH transcription factor 1 is required for the maintenance of leukemia stem cell in MLL-AF9+ acute myeloid leukemia

Project description:Twist family BHLH transcription factor 1 is required for the maintenance of leukemia stem cell in MLL-AF9+ acute myeloid leukemia

| PRJNA888092 | ENA

Expression data from murine Tet-off MLL-AF9/Ras acute myeloid leukemia cell lines following withdrawal of MLL-AF9

Project description:To explore oncogene addiction programs in a genetically defined leukemia context we developed an AML mouse model driven by a conditional MLL-AF9 allele together with oncogenic Ras, which enabled us to examine the consequences of MLL-AF9 inhibition in established disease. In order to produce a tightly regulated system that was easy to monitor, we constructed two retroviral vectors containing dsRed-linked MLL-AF9 under control of a tetracycline response element promoter, and KrasG12D or NrasG12D linked to the “Tet-off” tet-transactivator, which activates TRE expression in a doxycycline repressible manner. Leukemias were generated by retroviral cotransduction of both vectors into hematopoietic stem and progenitor cells, which were transplanted into syngeneic mice. Cells harboring both constructs induced aggressive myelomonocytic leukemia. Five independent primary leukemia cell lines were established from bone marrow of terminal mice. Treatment of these lines with doxycycline rapidly turned off MLL-AF9 expression, and induced terminal myeloid differentiation and complete disease remission in vivo. To identify molecular mechanisms underlying addiction to MLL-AF9, we analyzed global gene expression changes following doxycycline-induced suppression of MLL-AF9.

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Effect of loss of Jmjd1c on MLL-AF9 leukemia

Project description:Analysis of gene expression profile of MLL-AF9 leukemia cells 6 days after loss of Jmjd1c. Loss of Jmjd1c induces differentiation and apoptosis in MLL-AF9 leukemia cells. These results provide insight into the role of Jmjd1c in MLL leukemia.

2016-06-09 | GSE75576 | GEO

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