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RNA m6A methylation orchestrates cancer growth and metastasis via macrophage reprogramming

ABSTRACT: RNA m6A methylation orchestrates cancer growth and metastasis via macrophage reprogramming

PROVIDER: PRJNA667832 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12784380.fastq.gz	Fastqsanger.gz
	SRR12784381.fastq.gz	Fastqsanger.gz
	SRR12784382.fastq.gz	Fastqsanger.gz
	SRR12784383.fastq.gz	Fastqsanger.gz
	SRR12784384.fastq.gz	Fastqsanger.gz

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RNA m6A methylation orchestrates cancer growth and metastasis via macrophage reprogramming.

Project description:N6-methyladenosine (m6A) is a reversible mRNA modification that has been shown to play important roles in various biological processes. However, the roles of m6A modification in macrophages are still unknown. Here, we discover that ablation of Mettl3 in myeloid cells promotes tumour growth and metastasis in vivo. In contrast to wild-type mice, Mettl3-deficient mice show increased M1/M2-like tumour-associated macrophage and regulatory T cell infiltration into tumours. m6A sequencing reveals that loss of METTL3 impairs the YTHDF1-mediated translation of SPRED2, which enhances the activation of NF-kB and STAT3 through the ERK pathway, leading to increased tumour growth and metastasis. Furthermore, the therapeutic efficacy of PD-1 checkpoint blockade is attenuated in Mettl3-deficient mice, identifying METTL3 as a potential therapeutic target for tumour immunotherapy.

| S-EPMC7925544 | biostudies-literature

RNA m6A methylation orchestrates cancer growth and metastasis via macrophage reprogramming

Project description:The CD45+ immune-infiltrated cells in B16 tumors from WT or KO mice were enriched. Then, pooled samples of mice per group were analyzed by single cell RNA sequencing （scRNA-seq）

2021-01-19 | GSE159156 | GEO

A macrophage autonomous alpha4beta1integrin-Syk-Rac2 signaling axis controls macrophage differentiation, tumor growth and metastasis

Project description:Macrophages, play an essential role in promoting tumor growth by affecting angiogenesis, immune suppression, invasion and metastasis. The signal transduction events within macrophages which encode the complex cascade of events required for tumor growth and polarization of macrophages are poorly understood. We have discovered an ECM dependent signaling pathway in macrophages that regulates M2 macrophage differentiation, tumor growth, invasion and metastasis. We provide direct evidence that a macrophage autonomous, M-NM-14M-NM-21 integrin dependent Syk-Rac2 signaling axis acts in concert with the p110 isoform (PTEN-PI-3 kinase pathway) to control metastasis. Bone marrow derived macrophages from five wild type and five Rac2 -/- mutant C57BL mice.

2012-10-02 | E-GEOD-41236 | biostudies-arrayexpress

A conserved atypical MFS family member orchestrates a subset of O-glycosylation to facilitate macrophage dissemination and tissue invasion

Project description:Aberrant display of the truncated core1 O-glycan T-antigen is a common feature of human cancer cells that correlates with metastasis. Here we show that T-antigen in Drosophila melanogaster macrophages is involved in their developmentally programmed tissue invasion. Higher macrophage T-antigen levels require an atypical major facilitator superfamily (MFS) member that we named Minerva which enables macrophage dissemination and invasion. We characterize for the first time the T and Tn glycoform O-glycoproteome of the Drosophila melanogaster embryo, and determine that Minerva increases the presence of T-antigen on protein pathways previously linked to cancer, most strongly on the protein sulfhydryl oxidase Qsox1 which we show is required for macrophage invasion. Minerva’s vertebrate ortholog, MFSD1, rescues the minerva mutant’s migration and T-antigen glycosylation defects. We thus identify a key conserved regulator that orchestrates O-glycosylation on a protein subset to activate a program governing migration steps important for both development and cancer metastasis

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A macrophage autonomous Î±4Î²1integrin-Syk-Rac2 signaling axis controls macrophage differentiation, tumor growth and metastasis

Project description:Macrophages, play an essential role in promoting tumor growth by affecting angiogenesis, immune suppression, invasion and metastasis. The signal transduction events within macrophages which encode the complex cascade of events required for tumor growth and polarization of macrophages are poorly understood. We have discovered an ECM dependent signaling pathway in macrophages that regulates M2 macrophage differentiation, tumor growth, invasion and metastasis. We provide direct evidence that a macrophage autonomous, Î±4Î²1 integrin dependent Syk-Rac2 signaling axis acts in concert with the p110 isoform (PTEN-PI-3 kinase pathway) to control metastasis. SmoA1 Tg MB tumor cells were sorted into CD15+ and CD15- populations. RNA from these samples were hybridized to Affymetrix Mouse Genome 1.0 ST array.

2012-11-15 | E-GEOD-41717 | biostudies-arrayexpress

Menin orchestrates macrophage reprogramming to maintain the pulmonary immune homeostasis

Project description:Menin orchestrates macrophage reprogramming to maintain the pulmonary immune homeostasis

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Hypoxic stabilization of RIPOR3 mRNA via METTL3-mediated m6A RNA methylation drives breast tumor growth and metastasis [m6A-seq-T47D]

Project description:N6-methyladenosine (m6A) modification is the most abundant internal mRNA modification in eukaryotes. Hypoxia induces reprogramming of m6A epitranscriptome, but the detail underlying regulator mechanism remains elusive in breast cancer. Here we reported that hypoxia induced elevated m6A modification involved in tumor progression. m6A- sequencing (m6A-seq) combined with RNA sequencing (RNA-seq) identified RIPOR3 as a key target gene of m6A modification under hypoxic stress. Hypoxia-induced increased of RIPOR3 m6A levels promoted its mRNA stability and expression, thereby facilitating the progression and metastasis of breast cancer. Besides, RIPOR3 was overexpressed in breast cancer cells and breast tumor tissues, and elevation of RIPOR3 expression was associated with poor prognosis. Mechanistically, RIPOR3 bound to EGFR and the interaction was enhanced under hypoxia, promoting the activation of the EGFR downstream PI3K-AKT signaling pathway. Altogether, our studies reveal that RIPOR3 responds to hypoxic stress to promote EGFR-PI3K-AKT signal pathway, facilitating breast cancer progression and metastasis, thus presenting itself as a potential therapeutic target.

2024-10-04 | GSE264245 | GEO

Oxidative phosphorylation selectively orchestrates tissue macrophage homeostasis

Project description:Oxidative phosphorylation selectively orchestrates tissue macrophage homeostasis

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A macrophage autonomous alpha4beta1integrin-Syk-Rac2 signaling axis controls macrophage differentiation, tumor growth and metastasis

Project description:Macrophages, play an essential role in promoting tumor growth by affecting angiogenesis, immune suppression, invasion and metastasis. The signal transduction events within macrophages which encode the complex cascade of events required for tumor growth and polarization of macrophages are poorly understood. We have discovered an ECM dependent signaling pathway in macrophages that regulates M2 macrophage differentiation, tumor growth, invasion and metastasis. We provide direct evidence that a macrophage autonomous, α4β1 integrin dependent Syk-Rac2 signaling axis acts in concert with the p110 isoform (PTEN-PI-3 kinase pathway) to control metastasis.

2012-10-02 | GSE41236 | GEO

A macrophage autonomous α4β1integrin-Syk-Rac2 signaling axis controls macrophage differentiation, tumor growth and metastasis

Project description:Macrophages, play an essential role in promoting tumor growth by affecting angiogenesis, immune suppression, invasion and metastasis. The signal transduction events within macrophages which encode the complex cascade of events required for tumor growth and polarization of macrophages are poorly understood. We have discovered an ECM dependent signaling pathway in macrophages that regulates M2 macrophage differentiation, tumor growth, invasion and metastasis. We provide direct evidence that a macrophage autonomous, α4β1 integrin dependent Syk-Rac2 signaling axis acts in concert with the p110 isoform (PTEN-PI-3 kinase pathway) to control metastasis.

2012-11-15 | GSE41717 | GEO

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