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

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

PROVIDER: PRJNA1048058 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27030569_1.fastq.gz	Fastqsanger.gz
	SRR27030569_2.fastq.gz	Fastqsanger.gz
	SRR27030570_1.fastq.gz	Fastqsanger.gz
	SRR27030570_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 [RNA-seq]

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 | GSE249226 | GEO

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

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

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

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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 Carcinoma

2024-08-23 | PXD047673 | Pride

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

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

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

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

| PRJNA1048062 | ENA

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.

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Glucose-driven histone lactylation promotes the immunosuppressive activity of monocyte-derived macrophages in glioblastoma

Project description:Macrophages are critical components of the immunosuppressive microenvironment that restrict anti-cancer immunity in glioblastoma (GBM). However, how GBM shapes the regulatory function of macrophages remains elusive. Here, we report that monocyte-derived macrophages (MDM), but not yolk-sac derived microglia (MG), exhibited potent immunosuppressive activity, which was mediated by a population of glycolytic GLUT1+MDM, in an IL10-dependent manner. GBM-derived factors reprogrammed MDM towards glycolytic cells with enhanced avidity for glucose, which was mostly used to generate lactate. In turn, intracellular lactate caused lactylation of histone lysine residues that promoted MDM immunosuppressive activity via regulation of Il10 expression. GBM-primed activation of PERK supported glucose metabolism and regulated GLUT1 expression through ATF4 in MDM. PERK-deletion in MDM abrogated histone lactylation and suppressive activity, thereby promoting polyfunctional T cell-infiltration of tumors. In combination with immunotherapy, PERK-deletion blocked GBM progression. Our study demonstrates that glucose-driven histone lactylation controls MDM immunosuppressive function; all in a PERK-dependent manner.

2024-05-06 | GSE260700 | GEO

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