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We are analyzing https://www.nature.com/articles/s41467-021-21514-8.

Title:
RNA m6A methylation orchestrates cancer growth and metastasis via macrophage reprogramming | Nature Communications
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. N6-methyladenosine (m6A) is a reversible mRNA modification with important roles in cancer biology and immunoregulation. Here, the authors show that myeloid-specific deletion of Mettl3, the catalytic subunit of the methyltransferase complex, promotes tumor growth and metastasis in preclinical tumor models, influencing macrophage reprogramming and attenuating PD-1 blockade.
Website Age:
30 years and 10 months (reg. 1994-08-11).

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Keywords {🔍}

mice, cells, pubmed, bmdms, tumour, fig, mettl, article, cell, cas, google, scholar, macrophages, expression, data, supplementary, analysis, group, spred, tumours, central, tams, rna, mrna, nature, macrophage, growth, metastasis, stat, qrtpcr, shown, cancer, increased, experiments, immune, llc, nfκb, mettldeficient, results, depletion, microenvironment, injected, source, treg, tnfα, arg, lung, determined, representative, performed,

Topics {✒️}

nature portfolio privacy policy c-myc-mediated epigenetic silencing advertising national key research nf-κb/il-6/stat3 signalling axis starting research funding anti-ifn-γ-alexa fluor 647 social media development program hrp-conjugated anti-mouse igg middle panel pe-cy7-conjugated cd11b ab m6a-cd70-mediated immune suppression elisa kits apc-conjugated anti-f4/80 ab libraries reprints upregulated trkb/erk-mapk signaling xiangpeng wang & angang yang anti-tnf-α neutralizing antibodies specific pathogen-free conditions anti-phosphorylated nf-κb p65 received anti-cd25 antibodies research design paired-end fastq files nature 475 nature 513 nature 540 nature 566 nature 548 nature 552 nature gehan–breslow-wilcoxon test gehan–breslow–wilcoxon test tumour-derived lactic acid mapk pathway-related genes bone marrow-derived macrophage lps-induced inflammatory response canonical nf-κb signalling exogenous factor tnf-α p-body purification reveals myeloid-derived suppressor cells anti-cd11b-pe-cy7 promoter-bound mettl3 augments anti-cd25-pe-cy7 thermo fisher scientific research primescript qrt-pcr kit mettl3-deficient tams expressing

Schema {🗺️}

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      headline:RNA m6A methylation orchestrates cancer growth and metastasis via macrophage reprogramming
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      name:The State Key Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology, Fourth Military Medical University, Xi’an, China
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      name:Henan Key Laboratory of Immunology and Targeted Therapy, School of Laboratory Medicine, Xinxiang Medical University, Xinxiang, China
      name:Henan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, School of Laboratory Medicine, Xinxiang Medical University, Xinxiang, China
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      name:Henan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, School of Laboratory Medicine, Xinxiang Medical University, Xinxiang, China
      name:The State Key Laboratory of Cancer Biology, Department of Immunology, Fourth Military Medical University, Xi’an, China
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