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DNA methylation stochasticity is linked to transcriptional variability and identifies convergent epigenetic disruption across genetically-defined subtypes of AML [CellCulture_WGBS]

ABSTRACT: Epigenetic regulators are frequently mutated in acute myeloid leukemia (AML). We investigated DNA methylation stochasticity in genetic subtypes of AML using WGBS data and publicly-available ERRBS data, and identified transcriptional dysregulation and altered chromatin accessibility related to methylation entropy using single-cell RNA-seq and single-cell ATAC-seq data. We demonstrated that the hypomethylating drug decitabine (DAC) leads to reduction of DNA methylation entropy specifically in IDH2-mutant AML cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE319448 | GEO | 2026/03/09

REPOSITORIES: GEO

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DNA methylation stochasticity is linked to transcriptional variability and identifies convergent epigenetic disruption across genetically-defined subtypes of AML [scRNAseq]

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DNA methylation stochasticity is linked to transcriptional variability and identifies convergent epigenetic disruption across genetically-defined subtypes of AML [PrimaryAML_scATACseq]

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Gene expression profiling upon treatment with NTX-301

Project description:A novel hypomethylating agent NTX-301 is a promising therapeutic agent for AML patients. To examine its mechanisms of action, we produced gene expression data upon treatment with NTX-301 or decitabine (DAC) in AML cell lines.

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Upregulated cholesterol biosynthesis facilitates the survival of methylation-retaining AML cells following decitabine treatment [scNMT-Seq]

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Hypoxia impairs decitabine-induced expression of HLA-DR in acute myeloid leukaemia cell lines [Bisulfite-Seq]

Project description:Background Hypomethylating agents (HMA), such as azacytidine (AZA) and decitabine (DAC), are epigenetic therapies used to treat some patients with acute myeloid leukaemia (AML) and myelodysplastic syndrome (MDS). HMAs act in a replication-dependent manner to remove DNA methylation from the genome. However, AML cells targeted by HMA therapy are often quiescent within the bone marrow, where oxygen levels are low. In this study, we investigate the effects of hypoxia on HMA responses in AML cells. Results AML cell lines (MOLM-13, MV-4-11, HL-60) were treated with DAC (100nM) or AZA (500-2000nM) in normoxic (21% O2) and hypoxic (1% O2) conditions. Hypoxia significantly reduced AML cell growth and colony-forming capacity across all cell lines, with no additional effects observed upon HMA treatment. Hypoxia had no impact on the extent of DNA hypomethylation induced by DAC treatment, but limited AZA-induced loss of methylation from the genome. Transcriptional responses to HMA treatment were also altered, with HMAs failing to up-regulate antigen presentation pathways in hypoxia. In particular, cell surface expression of the MHC class II receptor, HLA-DR, was increased by DAC treatment in normoxia, but not hypoxia. Conclusion Our results suggest that HMA-induced antigen presentation may be impaired by hypoxia. This study highlights the need to consider microenvironmental factors when designing co-treatment strategies to improve HMA therapeutic efficacy.

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Hypoxia impairs decitabine-induced expression of HLA-DR in acute myeloid leukaemia cell lines [RNA-seq]

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DNA methylation profiling upon treatment with NTX-301 or decitabine in AML cells

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