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RNA sequestration in P-bodies sustains myeloid leukemia [RNA-seq]

ABSTRACT: We performed RNA-seq to profile transcriptional changes in AML cells following P-body dissolution induced by DDX6 knockdown.

ORGANISM(S): Homo sapiens

PROVIDER: GSE224748 | GEO | 2024/07/12

REPOSITORIES: GEO

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RNA sequestration in P-bodies sustains myeloid leukemia [ATAC-seq]

Project description:We performed ATAC-seq to profilechromatin changes in AML cells following P-body dissolution induced by DDX6 knockdown.

2024-07-12 | GSE224746 | GEO

RNA sequestration in P-bodies sustains myeloid leukemia [small RNA-seq]

Project description:To investigate small non-coding RNA changes in AML cells following loss of P-bodies, we knocked down DDX6 in MOLM-13 cells.

2024-07-12 | GSE224851 | GEO

RNA sequestration in P-bodies sustains myeloid leukaemia

Project description:Post-transcriptional mechanisms are fundamental safeguards of progenitor cell identity and are often dysregulated in cancer. Here, we identified regulators of P-bodies as crucial vulnerabilities in acute myeloid leukaemia (AML) through genome-wide CRISPR screens in normal and malignant haematopoietic progenitors. We found that leukaemia cells harbour aberrantly elevated numbers of P-bodies and show that P-body assembly is crucial for initiation and maintenance of AML. Notably, P-body loss had little effect upon homoeostatic haematopoiesis but impacted regenerative haematopoiesis. Molecular characterization of P-bodies purified from human AML cells unveiled their critical role in sequestering messenger RNAs encoding potent tumour suppressors from the translational machinery. P-body dissolution promoted translation of these mRNAs, which in turn rewired gene expression and chromatin architecture in leukaemia cells. Collectively, our findings highlight the contrasting and unique roles of RNA sequestration in P-bodies during tissue homoeostasis and oncogenesis. These insights open potential avenues for understanding myeloid leukaemia and potential therapeutic interventions.

2024-08-08 | GSE260919 | GEO

RNA sequestration in P-bodies sustains myeloid leukaemia

2024-08-08 | GSE224643 | GEO

The interplay between RNA sequestration in P-bodies and chromatin architecture sustains myeloid leukemia

Project description:To investigate chromatin remodeling in AML cells following loss of P-bodies, we knocked down DDX6 in MOLM-13 cells.

2024-08-09 | GSE224931 | GEO

RNA sequestration in P-bodies sustains myeloid leukemia [HSPC_RNAseq]

Project description:We performed RNA-seq to profile transcriptional changes in hematopoietic stem and progenitor cells following Ddx6 deletion.

2024-08-15 | GSE274860 | GEO

The interplay between RNA sequestration in P-bodies and chromatin architecture sustains myeloid leukemia [CUT&RUN]

Project description:To investigate chromatin remodeling in AML cells following loss of P-bodies, we knocked down DDX6 in MOLM-13 cells.

2024-08-11 | GSE261265 | GEO

RNA sequestration in P-bodies sustains myeloid leukemia [P-body-seq]

Project description:We performed RNA-seq to profile transcripts sequestered in P-bodies of AML cells

2024-07-12 | GSE224752 | GEO

RNA sequestration in P-bodies sustains myeloid leukemia

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-07-12 | GSE224858 | GEO

A PRC2-KDM5B-stemness regulatory axis sustains tumorigenicity of acute myeloid leukemia [RNA-Seq]

Project description:Acute myeloid leukemias (AMLs) with the NUP98-NSD1 or MLL gene rearrangement (MLL-r) share transcriptomic profiles featured with stemness-related gene signatures and display poor prognosis in the clinic. However, the molecular underpinnings of AML aggressiveness and stemness remain far from clear. Here, we report that the enzymatic activity of Polycomb Repressive Complex 2 (PRC2) is crucial for maintenance of tumorigenicity in NUP98-NSD1+ AML, consistent to its role in MLL-r AML. Transcriptomic analysis revealed Kdm5b, a lysine demethylase gene carrying the “bivalent domain” chromatin feature in AML, to be directly repressed by PRC2. While ectopic expression of Kdm5b suppressed AML growth, its depletion in AML not only promoted tumorigenicity but also significantly attenuated anti-AML effects by PRC2 inhibitors, thus demonstrating an involvement of the PRC2-|Kdm5b axis for AML oncogenesis. Lower KDM5B expression is positively correlated with poorer prognosis of human AML patients. RNA-seq, ChIP-seq and CUT&RUN based genomic profilings also showed that Kdm5b directly binds to and represses AML stemness genes. In contrast to an essential involvement for its various chromatin-associating domains, Kdm5b’s demethylase function was found to be dispensable for AML suppression, indicating a scaffold role in assembling gene-repressive complexes. Collectively, this study describes a molecular axis involving histone modifiers (PRC2 and Kdm5b) for sustaining the malignant features of AML, implicative of potential therapeutics.

2022-02-22 | GSE179167 | GEO

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