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RNA-seq analysis of BRD4 knockdown in U937 cells

ABSTRACT: Succinyl-CoA synthetase was reported to sustain mitochondrial respiration and enhance leukemia proliferation. However, the biological mechanisms of mitochondrial metabolism and leukemia pathogenesis, beyond energy production, remains underexplored. Here we report that depletion of SUCLG1 causes hypersuccinylation in leukemia cell lines, which impairs cell proliferation and leukemia progression. We hypothesize that increased histone H3 succinylation attenuates bromodomain interaction with chromatin, hence disrupting BRD4-mediated leukemogenic genes transcription. To confirm the hypothesis, we performed RNA-seq analysis in SUCLG1 knockout cell lines, JQ1-treated cells, Ksuc high and low primary AML patients.

ORGANISM(S): Homo sapiens

PROVIDER: GSE300338 | GEO | 2026/07/01

REPOSITORIES: GEO

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Succinyl-CoA synthetase deficiency in mouse forebrain results in hyper-succinylation with perturbed neuronal transcriptional regulation and metabolism (RNA-Seq)

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