SUCLG1-deficiency causes hypersuccinylation and impairs leukemia development [ChIP-seq]

ABSTRACT: Succinyl-CoA synthetase was reported to sustain mitochondrial respiration and enhance leukemia proliferation in acute myeloid leukemia (AML). 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 ChIP-seq analysis on BRD4 in SUCLG1 knockout cell lines.

ORGANISM(S): Homo sapiens

PROVIDER: GSE272739 | GEO | 2026/07/21

REPOSITORIES: GEO