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Global Lactylation Profiling Reveals Lactate-Driven Regulatory Mechanisms Promoting Tumor Progression in Oral Squamous Cell Carcinoma [CUT&TAG]

ABSTRACT: Global Lactylation Profiling Reveals Lactate-Driven Regulatory Mechanisms Promoting Tumor Progression in Oral Squamous Cell Carcinoma [CUT&TAG]

PROVIDER: PRJNA1048060 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27030616_1.fastq.gz	Fastqsanger.gz
	SRR27030616_2.fastq.gz	Fastqsanger.gz
	SRR27030617_1.fastq.gz	Fastqsanger.gz
	SRR27030617_2.fastq.gz	Fastqsanger.gz

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Global Lactylation Profiling Reveals Lactate-Driven Regulatory Mechanisms Promoting Tumor Progression in Oral Squamous Cell Carcinoma [CUT&TAG]

Project description:Cancer cells often rely on aerobic glycolysis for metabolism, and lactylation, a newly discovered post-translational modification, significantly impacts molecular processes. This study comprehensively analyzes lactylation's role in oral squamous cell carcinoma (OSCC), providing initial insights into its impact on progression. Oral squamous cell carcinoma cell lines, before and after lactate treatment, underwent CUT&TAG, ATAC, and transcriptomic sequencing. ChIP-qPCR and RT-qPCR validated results in OSCC tissues. Integrated analysis identified 217 genes with increased expression driven by lactylation in OSCC. Lactylation broadly impacted pathways in cancer, notably regulating PI3K/AKT and MAPK signaling. This pioneering study analyzes lactylation in OSCC, providing a global map of its regulation in oral squamous cell carcinoma from the perspective of chromatin-driven gene expression.

2024-08-20 | GSE249224 | GEO

Global Lactylation Profiling Reveals Lactate-Driven Regulatory Mechanisms Promoting Tumor Progression in Oral Squamous Cell Carcinoma [ATAC-seq]

2024-08-20 | GSE249223 | GEO

Global Lactylation Profiling Reveals Lactate-Driven Regulatory Mechanisms Promoting Tumor Progression in Oral Squamous Cell Carcinoma [RNA-seq]

2024-08-20 | GSE249226 | GEO

Lactate regulates cell differentiation of erythroid progenitor cells via histone lactylation modification [CUT&Tag]

Project description:As a key metabolite of glycolysis, lactate plays important regulatory roles in a variety of biological events by regulating metabolic homeostasis and histone lactylation. However, the role of lactate and histone lactylation in human erythropoiesis remains unclear. Here, we explored the role of lactate in erythropoiesis by adding the glycolysis inhibitor 2-DG or exogenous lactate Na-La to decrease or increase intracellular lactate levels, respectively. The results showed that 2-DG treatment promoted erythroid progenitors differentiation, blocked cell cycle and reduced colony-forming ability of CFU-E. In contrast, Na-La delayed erythroid progenitors differentiation and promoted CFU-E colony formation. We also found that lactate levels directly regulated H3K14la and H3K18la intensity. Furthermore, CUT&Tag results showed that the lost H3K14la peaks after 2-DG treatment were mainly enriched in promoter region and were associated with cell cycle and division. RNA-seq results showed that gene expression pattern was dramatically altered after 2-DG treatment, and differentially expressed genes were enriched in cell cycle and division process. Integrated analysis of CUT&Tag and RNA-seq revealed that gene expression was regulated by H3K14la, and CCNB1, CFL1, CENPA, SKA2 and GNAI2 gene expression were verified by RT-qPCR. In conclusion, our study reveals that lactate affects the cell differentiation of early erythroid progenitors by regulating gene expression through histone lactylation.

2025-05-17 | GSE274165 | GEO

Hexokinase 2 and lactate mediated gene expression via histone H3 lysine 18 lactylation (CHO CUT&Tag)

Project description:Hexokinase catalyzes the first committed step in glucose metabolism by phosphorylating glucose to produce glucose-6-phosphate. Highly glycolytic proliferating cells such as cancer cells take advantage of HK2 expression to accelerate glucose metabolism even in the presence of oxygen. This acceleration not only provides sufficient glycolytic intermediates to support the anabolic demands of the cells but also inevitably accompanies increased formation of metabolic end products such as lactate. Currently, the effect of lactate caused by HK2-mediated metabolic alteration is largely unknown. A recent study found that lactate plays a role in an epigenetic alteration known as histone lactylation. Here, using RNA-seq and CUT&Tag chromatin profiling, we study the effect of HK2 and lactate on gene expression via histone lactylation (H3K18la).

2023-05-05 | GSE229151 | GEO

Tumor-associated macrophage-derived lactate remodels glioblastoma immune microenvironment through regulation of NHEJ repair by KU70 lactylation

Project description:Glioblastoma (GBM) is a malignancy with a complex tumor microenvironment (TME) dominated by glioblastoma stem cells (GSCs) and infiltrated by tumor-associated macrophages (TAMs), and exhibits aberrant metabolic pathways. Lactate is a critical glycolytic metabolite that promotes tumor progression; however, the mechanisms of lactate transportation and lactylation in the tumor microenvironment (TME) of GBM remain elusive. Here, we found that the lactate metabolic signature was highly expressed in TAMs and tumor cells. Moreover, TAMs provide lactate to GSCs, promoting GSC proliferation and inducing lactylation of the non-homologous end joining (NHEJ) protein KU70 at the residue K317. TAM-derived lactate-mediated KU70 lactylation inhibits cGAS- type I interferon signaling, remodeling the immunosuppressive microenvironment through reduced cytotoxic CD8+ T cell infiltration, promoting the malignant progression of GBM. Combinatorial targeting of lactate transport and immune checkpoints demonstrated additive therapeutic benefit in immunocompetent orthotopic xenograft models. This study unveils TAM-derived lactate and lactylation as a critical regulator of NHEJ and create immunosuppressive microenvironment, linking the TME to DNA damage response in GBM and opening novel avenues for developing combinatorial therapy for GBM.

2024-06-01 | GSE266884 | GEO

Lactate regulates cell differentiation of erythroid progenitor cells via histone lactylation modification [RNA-seq]

2025-05-17 | GSE274169 | GEO

Global Lactylation Profiling Reveals Lactate-Driven Regulatory Mechanisms Promoting Tumor Progression in Oral Squamous Cell Carcinoma

Project description:Global Lactylation Profiling Reveals Lactate-Driven Regulatory Mechanisms Promoting Tumor Progression in Oral Squamous Cell Carcinoma

| PRJNA1048061 | ENA

Global Lactylation Profiling Reveals Lactate-Driven Regulatory Mechanisms Promoting Tumor Progression in Oral Squamous Cell Carcinoma

2024-08-23 | PXD047535 | Pride

Lactate-Driven Protein Lactylation Regulates Virulence in Plasmodium falciparum

Project description:Lactic acidosis, driven by hyperlactatemia, is a hallmark of severe Plasmodium falciparum malaria, yet its impact on parasitic life cycle and gene expression remains unclear. In mammalian cells, lactate influences transcription through histone lactylation, a novel post-translational modification. In this study, we demonstrate that P. falciparum undergoes lactate-derived lysine lactylation on nuclear proteins, including histones, histone variants, and AP2 transcription factors, with lactylation levels dynamically varying in response to physiological lactate ranges. Through CUT&RUN profiling, we show that elevated lactate enhances chromatin occupancy of lactylated proteins at promoters of genes involved in virulence and cytoadherence. Correspondingly, transcriptomic analyses demonstrated a suppression of these genes in response to elevated lactate, a pattern also evident in clinical isolates from severe malaria patients. Functionally, we demonstrate that high lactate reduces the binding ability of infected erythrocytes to CD36 receptor. Together, our findings reveal protein lactylation as a metabolite-responsive epigenetic mechanism in P. falciparum, linking host metabolic state to transcriptional reprogramming with direct implications for parasite virulence and disease pathogenesis.

2025-08-08 | GSE304394 | GEO

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