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Lactate regulates major zygotic genome activation by H3K18 lactylation in mammals

ABSTRACT: Lactate regulates major zygotic genome activation by H3K18 lactylation in mammals

PROVIDER: PRJNA979204 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24821167_1.fastq.gz	Fastqsanger.gz
	SRR24821167_2.fastq.gz	Fastqsanger.gz
	SRR24821168_1.fastq.gz	Fastqsanger.gz
	SRR24821168_2.fastq.gz	Fastqsanger.gz
	SRR24821169_1.fastq.gz	Fastqsanger.gz

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Lactate regulates major zygotic genome activation by H3K18 lactylation in mammals [RNA-seq]

Project description:Lactate regulates major zygotic genome activation by H3K18 lactylation in mammals [RNA-seq]

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Lactate regulates major zygotic genome activation by H3K18 lactylation in mammals [CUT&TAG]

Project description:Lactate regulates major zygotic genome activation by H3K18 lactylation in mammals [CUT&TAG]

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Lactate regulates major zygotic genome activation by H3K18 lactylation in mammals [CUT&TAG]

Project description:Lactate is present at a high level in the microenvironment of mammalian preimplantation embryos in vivo and in vitro. However, its role in preimplantation development is unclear. Here, we report that lactate is highly enriched in the nuclei of early embryos when major zygotic genome activation (ZGA) occurs in humans and mice. The inhibition of its production and uptake results in developmental arrest at the 2-cell stage, major ZGA failure, and loss of lactate-derived H3K18lac, and the abnormal phenotypes could be recapitulated by overexpression of H3K18R mutation and rescued by addition of Lac-CoA. By profiling the landscape of H3K18lac in human and mouse preimplantation embryos, we show that H3K18lac is enriched on the promoter regions of most major ZGA genes and corelates with their expressions. Taken together, we demonstrate the important role for lactate in major ZGA via H3K18lac, showing a conserved metabolic mechanism underlies preimplantation development of mammalian embryos.

2024-02-14 | GSE234026 | GEO

Lactate regulates major zygotic genome activation by H3K18 lactylation in mammals [RNA-seq]

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Lactate regulates major zygotic genome activation by H3K18 lactylation in mammals

Project description: Not available

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Lactate promotes cholesterol uptake by facilitating SCARB1 expression through histone H3K18 lactylation

Project description:Lactate promotes cholesterol uptake by facilitating SCARB1 expression through histone H3K18 lactylation

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Lactate regulates major zygotic genome activation by H3K18 lactylation in mammals

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

2024-02-14 | GSE234027 | GEO

Lactate promotes cholesterol uptake by facilitating SCARB1 expression through histone H3K18 lactylation

Project description:Metabolic reprogramming supports the proliferation of cancer cells under hypoxic stress, including enhanced glycolysis and altered fatty acid metabolism. However, the mechanism underlying its regulation of cholesterol metabolism remains incompletely understood. Here, we show that lactate-induced cholesterol accumulation activates mammalian target of rapamycin complex 1 (mTORC1) signaling under hypoxic conditions, thereby promoting hepatocellular carcinoma (HCC) progression. Mechanistically, lactate upregulates scavenger receptor class B type 1 (SCARB1) expression by enhancing histone H3 lysine 18 lactylation (H3K18la), leading to increased cholesterol levels. We furthermore demonstrate that SCARB1-mediated cholesterol uptake is essential for the activation of mTORC1, which promotes tumor growth by preventing HCC cells from excessive autophagy. Importantly, analysis of clinical HCC samples showed a positive correlation between H3K18la and SCARB1 expression. Taken together, these findings provide novel insights into hypoxia-driven metabolic reprogramming and reveal a previously unrecognized connection between lactate and cholesterol metabolism, suggesting a potential innovative cancer therapy for HCC.

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Cancer-Associated Fibroblasts Shape a High-Lactate Microenvironment to Drive Perineural Invasion in Pancreatic Cancer via Histone Lactylation

Project description:Perineural invasion (PNI) is a pivotal prognostic factor in pancreatic cancer, associated with aggressive tumor behavior and adverse patient outcomes. Despite its recognized clinical impact, the molecular mechanisms underlying PNI are not well understood. In this study, we isolated perineural invasion-associated cancer-associated fibroblasts (pCAFs), which demonstrated a markedly enhanced capacity to promote neural invasion in pancreatic cancer compared to non-perineural invasion-associated CAFs (npCAFs). Utilizing single-cell, high-throughput sequencing, and metabolomics, we identified a significant upregulation of glycolysis in pCAFs, fostering a high-lactate tumor microenvironment conducive to cancer progression. pCAFs-derived lactate is absorbed by tumor cells, facilitating histone H3K18 lactylation. This epigenetic modification activates the transcription of neural invasion-associated genes such as L1CAM and SLIT1, thereby driving PNI in pancreatic cancer. Further exploration of metabolic reprogramming in pCAFs revealed enhanced acetylation of the glycolytic enzyme GAPDH, correlated with increased enzymatic activity and glycolytic flux. Targeting of GAPDH and lactylation modifications significantly inhibits neural invasion in a KPC mouse model. Clinical data suggested that high levels of H3K18 lactylation correlate with severe PNI and poorer patient prognosis. Our findings provide critical insights into the role of pCAFs in the PNI of pancreatic cancer, highlighting glycolytic reprogramming and lactate-driven histone modifications as potential therapeutic targets for PDAC.

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