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Distinct transcriptional signatures in mIDH leukemia cells as compared to wild type

ABSTRACT: Distinct transcriptional signatures in mIDH leukemia cells as compared to wild type

PROVIDER: PRJNA775975 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16611611_1.fastq.gz	Fastqsanger.gz
	SRR16611611_2.fastq.gz	Fastqsanger.gz
	SRR16611612_1.fastq.gz	Fastqsanger.gz
	SRR16611612_2.fastq.gz	Fastqsanger.gz
	SRR16611613_1.fastq.gz	Fastqsanger.gz

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Distinct transcriptional signatures in mIDH leukemia cells as compared to wild type

Project description:We report the results of bulk RNA sequencing on both parental and mIDH2R140Q TF-1 cell lines. We obtained 1 million cells of each cell line and extracted RNA to generate libraries. Our sequencing was performed with Novogene assistance. Differentially expressed genes (DEGs) were analyzed using DEseq2. Ultimately, we compared the expression of NF-κB targets and our results indicated upregulation of IL-1, IFNα and IFNγ in the mIDH2 cell line as compared to parental. Additionally using GSEA software, we noted increased expression of upstream and downstream constituents of the NF-κB pathway. This component of our study indicates the broad transcriptional changes induced by mIDH2R140Q mutation and demonstrates the upregulation of NF-κB specifically.

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Phosphoproteomics and Proteomics of wild-type and TauT-/- leukemia cells

Project description:Signals from the microenvironment are known to be critical for development, sustaining adult stem cells, and for oncogenic progression. While candidate niche-driven signals that can promote cancer progression have been identified, concerted efforts to comprehensively map microenvironmental ligands for cancer stem cell specific surface receptors have been lacking. Here, we use temporal single cell RNA-sequencing to identify molecular cues from the bone marrow stromal niche that engage leukemia stem cells (LSC) during oncogenic progression. We integrate these data with our RNA-seq analysis of human LSCs from distinct aggressive myeloid cancer subtypes and our CRISPR based in vivo LSC dependency map7 to develop a temporal receptor-ligand interactome essential for disease progression. These analyses identify the taurine transporter (TauT)-taurine axis as a critical dependency of myeloid malignancies. We show that taurine production is restricted to the osteolineage population during cancer initiation and expansion. Inhibiting taurine synthesis in osteolineage cells impairs LSC growth in vitro and improves survival outcomes in vivo. Using TauT genetic loss of function murine models and patient-derived AML cells, we show that TauT inhibition significantly impairs in vivo myeloid leukemia progression. Consistent with elevated TauT expression in venetoclax resistant AML, TauT inhibition synergizes with venetoclax to block growth of primary human AML cells. Mechanistically, our metabolomic, proteomic and transcriptomic approaches indicate that loss of taurine uptake inhibits Rag-GTP dependent mTOR activation and downstream glycolytic metabolism. Collectively, our work establishes the temporal landscape of stromal signals during leukemia progression and identifies taurine as an important regulator of myeloid malignancies.

2025-03-28 | PXD062322 | Pride

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Project description:INTRODUCTION: Frontotemporal dementia (FTD) is characterized by progressive atrophy of frontal and/or temporal cortices and considerable clinical, pathological, and genetic heterogeneity. METHODS: Frontal and temporal cortex tissues from FTD-GRN (n=9), FTD-MAPT (n=13), and non-demented controls (n=11) were analysed with quantitative proteomics (DIA). Expression-weighted cell type enrichment deduced the role of major brain cell types and gene ontology analysis identified distinct biological processes. FTD-MAPT data was also compared to an AD (n=10) protein signature. RESULTS: We identified brain region-specific FTD protein expression signatures. In frontal cortex of FTD-GRN, we observed immune processes in endothelial cells and mitochondrial dysregulation in neurons. In temporal cortex of FTD-MAPT, we observed dysregulated RNA processing, oligodendrocyte dysfunction, and axonal impairment. Comparison with AD indicated that alterations in RNA processing and oligodendrocyte function are distinct for FTD-MAPT. DISCUSSION: Our results indicate cell type-specific biological processes distinctive for genetic FTD subtypes. These findings may aid the development of FTD subtype-specific treatment strategies.

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