RNA profiling of IL-34 overexpressing acute myeloid leukemia (AML) cells
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ABSTRACT:
PROVIDER: PRJNA879750 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21534608_1.fastq.gz | Fastqsanger.gz | |||
| SRR21534608_2.fastq.gz | Fastqsanger.gz | |||
| SRR21534609_1.fastq.gz | Fastqsanger.gz | |||
| SRR21534609_2.fastq.gz | Fastqsanger.gz | |||
| SRR21534610_1.fastq.gz | Fastqsanger.gz |
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Project description:Acute myeloid leukemia (AML) is a highly heterogeneous disease. In our study, we found that overexpressing IL-34 in AML cells accelerates the AML progression and shorten the mice survival, which is medicated by LSC level. We used one of the LSC markers, c-Kit, to divide AML cells. The goals of this study aim to reveal the mechanism mediated by IL-34 overexpression, we performed the RNAseq profiling of MA9-c-kit-, MA9-c-kit+ and MA9-IL-34 AML cells.
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Project description:Aberrant activation of β-catenin is a common event in Acute Myeloid Leukemia (AML), and is recognized as an independent predictor of poor prognosis. Although increased β-catenin signaling in AML has been associated with AML1-ETO and PML-RARα translocation products, and activating mutations in the FLT3 receptor, it remains unclear which mechanisms activate β-catenin in AML more broadly. Here, we describe a novel link between interleukin-3 (IL-3) signaling and the regulation of β-catenin in myeloid transformation and AML. Using a murine model of HoxB8 and IL-3 cooperation we show that IL-3 modulates β-catenin protein levels, and Cre-induced deletion of β-catenin abolishes IL-3 dependent growth and colony formation. In the erythroleukemic cell line TF-1.8, we observed increased β-catenin protein levels and nuclear localization in response to IL-3, which correlated with transcriptional induction of β-catenin target genes. Furthermore, IL-3 promoted β-catenin accumulation in a subset of AML patient samples, and microarray gene expression analysis of these cells revealed induction of WNT/β-catenin and TCF4 transcriptional gene signatures in an IL-3 dependent manner. This study is the first to link β-catenin activation to IL-3 and suggests that targeting IL-3 signaling may be an effective approach for the inhibition of β-catenin activity in some patients with AML. AML patient samples (AML1-4) were cultured in the presence or absence of hIL-3 for 6 or 16h.
2014-02-13 | E-GEOD-51402 | biostudies-arrayexpress
Project description:The paper describes a model of acute myeloid leukaemia.
Created by COPASI 4.26 (Build 213)
This model is described in the article:
Optimal control of acute myeloid leukaemia
Jesse A. Sharp, Alexander P Browning, Tarunendu Mapder, Kevin Burrage, Matthew J Simpson
Journal of Theoretical Biology 470 (2019) 30–42
Abstract:
Acute myeloid leukaemia (AML) is a blood cancer affecting haematopoietic stem cells. AML is routinely treated with chemotherapy, and so it is of great interest to develop optimal chemotherapy treatment strategies. In this work, we incorporate an immune response into a stem cell model of AML, since we find that previous models lacking an immune response are inappropriate for deriving optimal control strategies. Using optimal control theory, we produce continuous controls and bang-bang controls, corre- sponding to a range of objectives and parameter choices. Through example calculations, we provide a practical approach to applying optimal control using Pontryagin’s Maximum Principle. In particular, we describe and explore factors that have a profound influence on numerical convergence. We find that the convergence behaviour is sensitive to the method of control updating, the nature of the control, and to the relative weighting of terms in the objective function. All codes we use to implement optimal control are made available.
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Please refer to CC0 Public Domain Dedication for more information.
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Project description:Chromatin immunoprecipitation with specific isolation of chromatin associated proteins (ChIP-SICAP) was used to identify chromatin-bound interactors of CEBPA and RUNX1 in the 3q-rearranged human myeloid leukemia cell line HNT-34.
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Project description:Interleukin-34 (IL-34) is an alternative ligand to colony-stimulating factor-1 (CSF-1) for the CSF-1 receptor that acts as a key regulator of monocyte/macrophage lineage. In this study, we show that cancer cells-derived IL-34 mediates resistance to immune checkpoint blockade regardless of CSF-1 existence. In a therapeutic study of a programmed death-1 and cytotoxic T-lymphocyte-associated antigen-4 blocking monoclonal antibody, the expression of IL-34 in tumors was accompanied with limited benefits compared to IL-34 non-expressing tumors in various murine cancer models. Consistent with its immunosuppressive characteristics, the expression of IL-34 in tumors correlates with decreased frequencies of cellular (such as CD8+ and CD4+ T cells) and molecular (including various cytokines and chemokines) effectors at the tumor microenvironment. In addition, IL-34 blockade expands the M1-macrophage population. Then, a neutralizing antibody against IL-34 helped to reverse these effects and improved the therapeutic effects of the immune checkpoint blockade in combinatorial therapeutic models, including a patient-derived xenograft model of primary lung adenocarcinoma. Collectively, we revealed that tumor-derived IL-34 inhibits the efficacy of immune checkpoint blockade and proposed the utility of IL-34 blockade as a new strategy for cancer therapy.
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Project description:IL-34-differenciated CD14+CD115+ monocytes expand and potentiate IL-34+ Tregs to control human transplant rejection
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Project description:Aberrant activation of β-catenin is a common event in Acute Myeloid Leukemia (AML), and is recognized as an independent predictor of poor prognosis. Although increased β-catenin signaling in AML has been associated with AML1-ETO and PML-RARα translocation products, and activating mutations in the FLT3 receptor, it remains unclear which mechanisms activate β-catenin in AML more broadly. Here, we describe a novel link between interleukin-3 (IL-3) signaling and the regulation of β-catenin in myeloid transformation and AML. Using a murine model of HoxB8 and IL-3 cooperation we show that IL-3 modulates β-catenin protein levels, and Cre-induced deletion of β-catenin abolishes IL-3 dependent growth and colony formation. In the erythroleukemic cell line TF-1.8, we observed increased β-catenin protein levels and nuclear localization in response to IL-3, which correlated with transcriptional induction of β-catenin target genes. Furthermore, IL-3 promoted β-catenin accumulation in a subset of AML patient samples, and microarray gene expression analysis of these cells revealed induction of WNT/β-catenin and TCF4 transcriptional gene signatures in an IL-3 dependent manner. This study is the first to link β-catenin activation to IL-3 and suggests that targeting IL-3 signaling may be an effective approach for the inhibition of β-catenin activity in some patients with AML.
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Project description:Acute Myeloid Leukemia (AML) patient xenografts
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Project description:EVI1 is one of the famous poor prognostic markers for a chemotherapy-resistant acute myeloid leukemia (AML). To identify molecular targets on the surface of leukemia cells with EVI1high expression, we compared the gene expression profiles of several AML cell lines by DNA microarray To search for novel molecular targets in refractory myeloid leukemia with high EVI1 expression, we initially analyzed the gene expression profiles of 12 human myeloid cell lines. Four cell lines with chromosome 3q26 abnormalities (UCSD/AML1, HNT-34, Kasumi-3 and MOLM-1) expressed EVI1High, and eight myeloid cell lines without chromosome 3q26 abnormalities (HEL, HL-60, K052, THP-1, FKH-1, K051, NH and OIH-1) expressed low levels of EVI1 (EVI1Low)
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