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Epigenetic regulation of the acute T cell leukemia

ABSTRACT: Epigenetic regulation of the acute T cell leukemia

PROVIDER: PRJNA521525 | ENA |

REPOSITORIES: ENA

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Epigenetic regulation of the acute T cell leukemia

Project description:Treatment of the acute T cell leukemia cell line Jurkat in vitro with the most potent histone deacetylase inhibitor, Trichostatin A induced apoptosis in a dose-dependent manner. Analysis of the drug-treated Jurkat cells using high throughput genome-wide gene expression profiling indicated the upregulation as well as downregulation of several genes crucial for cellular functions. Use of quantitative reverse transcriptase-mediated polymerase chain reaction validated the regulation of selected genes in drug-treated cells. Collectively, this study has unraveled the genes involved in epigenetic regulation of the T cell leukemia. Microarray analysis was performed to determine the changes in global gene expression profiles during apoptosis of a T cell leukemia induced by the histone deacetylase inhibitor, Trichostatin A. Drug treatment induced the upregulation and repression of a number of genes.

2019-02-09 | GSE126315 | GEO

Epigenetic studies in Acute Myeloid Leukemia

Project description:Epigenetic studies in Acute Myeloid Leukemia

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CHMP5-Mediated Transcriptional Regulation of T-Cell Acute Lymphoblastic Leukemia

Project description:CHMP5-Mediated Transcriptional Regulation of T-Cell Acute Lymphoblastic Leukemia

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Profiling histone post-translational modifications to identify signatures of epigenetic drug response in T-cell acute lymphoblastic leukemia

Project description:Epigenetic modifications are dynamic and reversible, making them attractive targets for therapeutic intervention in cancer. Although several epigenetic drugs (epidrugs) have been clinically approved, their application in T-cell acute lymphoblastic leukemia (T-ALL) remains limited, and predictive biomarkers of response are lacking. Here, we present a mass spectrometry (MS)-based pharmacoepigenetic approach to profile histone post-translational modifications (hPTMs) to identify signatures associated with epidrug sensitivity in T-ALL. Baseline hPTM landscapes were previously established by our group for 21 T-ALL cell lines using liquid chromatography–tandem mass spectrometry (LC–MS/MS). Here, we treated these cell lines with a panel of nine epidrugs including anthracyclines, histone deacetylase inhibitors, and DNA methyltransferase inhibitors. Correlation of cell viability data with hPTM levels revealed distinct hPTM signatures linked to sensitivity for each drug class. These signatures were subsequently evaluated in T-ALL patient-derived xenograft (PDX) models. However, we our analysis revealed substantial discepancies in hPTM sensitivity signatures compared to those observed in vitro. Co-variation network analysis highlighted divergence in hPTM-hPTM correlation between the two models, underscoring limitations of cell lines for modeling dynamic epigenetic regulation in vivo. Our findings establish a framework for MS-based hPTM profiling in T-ALL and emphasize the importance of model selection in developing predictive epigenetic biomarkers.

2026-06-08 | PXD067935 | Pride

Epigenetic Control over IFN Type-I Response antagonizes self-renewal in acute myeloid leukemia

Project description:Large biological heterogeneity hallmarks acute myeloid leukemia (AML) and substantially hampers development of novel comprehensive therapies. While all-trans retinoic acid (ATRA) revolutionized therapy of acute promyelocytic leukemia, its impact on other AML subtypes remained largely disappointing. Here we show for the first time that ATRA mediated phosphorylation of the histone demethylase PHF8 induces apoptosis of AML cells of different subtypes via regulation of viral mimicry and subsequent initiation of interferon (IFN) type-I response. Phospho-PHF8 conferred H3K9me2 demethylation at promoter sites of key initiators of cell-intrinsic immune response. Multiomics based analyses revealed activation of cytosolic RNA sensors as key step towards NF-κB driven IFN type-I mediated apoptosis. Epigenetic changes directed by PHF8 also induced a specific proteosome pathway controlling NF-κB activity after its initial activation. Hence, PHF8 orchestrates viral mimicry, triggering IFN type-I response-differentiation-apoptotic network in a broad spectrum of AML when activated by ATRA. Forced phosphorylation of PHF8 via combination treatment with ATRA and simultaneous pharmacological inhibition of PHF8 dephosphorylation significantly impaired growth of human AML. Our findings finally open the gate for successful application of ATRA-based combination therapies in AML.

2024-06-22 | PXD035635 | Pride

CHMP5-Mediated Transcriptional Regulation of T-Cell Acute Lymphoblastic Leukemia (CHIPseq)

Project description:CHMP5-Mediated Transcriptional Regulation of T-Cell Acute Lymphoblastic Leukemia (CHIPseq)

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miRNA-1 promotes Acute Myeloid Leukemia cell pathogenesis through metabolic regulation

Project description:miRNA-1 promotes Acute Myeloid Leukemia cell pathogenesis through metabolic regulation

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CHMP5-Mediated Transcriptional Regulation of T-Cell Acute Lymphoblastic Leukemia (Murine RNAseq)

Project description:CHMP5-Mediated Transcriptional Regulation of T-Cell Acute Lymphoblastic Leukemia (Murine RNAseq)

| PRJNA1021646 | ENA

miRNA-1 promotes Acute Myeloid Leukemia cell pathogenesis through metabolic regulation [mRNA]

Project description:miRNA-1 promotes Acute Myeloid Leukemia cell pathogenesis through metabolic regulation [mRNA]

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CHMP5-Mediated Transcriptional Regulation of T-Cell Acute Lymphoblastic Leukemia (Human RNAseq)

Project description:CHMP5-Mediated Transcriptional Regulation of T-Cell Acute Lymphoblastic Leukemia (Human RNAseq)

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