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Superenhancer-driven lncRNA FASRL in hepatocellular carcinoma [ChIP-seq]

ABSTRACT: Superenhancers drive abnormal gene expression in tumors and promote malignancy. However, the relationship between superenhancer-associated lncRNA and abnormal metabolism is unknown.

ORGANISM(S): Homo sapiens

PROVIDER: GSE206547 | GEO | 2023/01/12

REPOSITORIES: GEO

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Superenhancer-driven lncRNA FASRL in hepatocellular carcinoma [RNA-seq]

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Superenhancer-driven lncRNA FASRL in hepatocellular carcinoma

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MAF converts metabolic state into superenhancer architecture and dependency in myeloma [ChIP-Seq]

Project description:Lineage-specific transcription factors govern superenhancer assemblies that impose extreme transcriptional output, but how metabolic capacity sustains these regulatory hubs remains unresolved. By integrating metabolomic, epigenomic and chromatin architecture analyses, we identify a previously unrecognized role for MAF in metabolically driven histone acetylation, including the superenhancer-defining mark H3K27ac, through enhanced acetyl-CoA availability derived from rewired glutamine anaplerosis. The channeling of acetylation donors to high-demand enhancer microdomains is facilitated by nucleus-localizing metabolic enzyme citrate synthase, thereby alleviating metabolically constrained chromatin states. This process is further reinforced by MAF-dependent transcriptional regulation of the rate-limiting acetyltransferase p300, culminating in a globally elevated yet spatially precise hyperacetylated chromatin landscape that drives expression of core myeloma oncogenes. Yet, this metaboloepigenetic coupling comes at the cost of conditional vulnerability, unmasking superenhancers as liabilities that can be selectively destabilized with dietary nutrient restriction, as exemplified by the superenhancer-encoded dependency ZC3H3. Our study thus highlights an underappreciated dimension of superenhancer biology, positioning MAF as a metabolic gatekeeper of enhancer function.

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Upregulation of Superenhancer-Driven LncRNA FASRL by USF1 Promotes De Novo Fatty Acid Biosynthesis to Exacerbate Hepatocellular Carcinoma.

Project description:Superenhancers drive abnormal gene expression in tumors and promote malignancy. However, the relationship between superenhancer-associated long noncoding RNA (lncRNA) and abnormal metabolism is unknown. This study identifies a novel lncRNA, fatty acid synthesis-related lncRNA (FASRL), whose expression is driven by upstream stimulatory factor 1 (USF1) through its superenhancer. FASRL promotes hepatocellular carcinoma (HCC) cell proliferation in vitro and in vivo. Furthermore, FASRL binds to acetyl-CoA carboxylase 1 (ACACA), a fatty acid synthesis rate-limiting enzyme, increasing fatty acid synthesis via the fatty acid metabolism pathway. Moreover, the expression of FASRL, USF1, and ACACA is increased, and their high expression indicates a worse prognosis in HCC patients. In summary, USF1 drives FASRL transcription via a superenhancer. FASRL binding to ACACA increases fatty acid synthesis and lipid accumulation to mechanistically exacerbate HCC. FASRL may serve as a novel prognostic marker and treatment target in HCC.

| S-EPMC9811444 | biostudies-literature

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