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METTL3-dependent m6A methylation in atherogenic endothelial inflammation [eCLIP]

ABSTRACT: Atherosclerosis is initiated by endothelial inflammation. Using RNA-seq and eCLIP, we identified METTL3 as a mechanosensitive m6A writer that upregulates NLRP1 and downregulates KLF4 through YTHDF readers. Knockdown of METTL3 abrogated these changes and protected against flow-induced atherogenesis in vitro and in vivo.

ORGANISM(S): Homo sapiens

PROVIDER: GSE298183 | GEO | 2026/06/26

REPOSITORIES: GEO

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METTL3-dependent m6A methylation in atherogenic endothelial inflammation [RNA]

Project description:Atherosclerosis is initiated by endothelial inflammation. Using RNA-seq and eCLIP, we identified METTL3 as a mechanosensitive m6A writer that upregulates NLRP1 and downregulates KLF4 through YTHDF readers. Knockdown of METTL3 abrogated these changes and protected against flow-induced atherogenesis in vitro and in vivo.

2026-06-26 | GSE298180 | GEO

mRNA-seq of neuronal compartments in shRNA-mediated + small-molecule knockdown of Mettl3 in mouse primary cortical neurons (mPCN)

Project description:To study the effect of m6A modifications on subcellular mRNA localization we depleted m6A writer Mettl3 with shRNA and small molecule from mouse primary cortical neurons (mPCN) and sequenced neuritic and somatic compartments in parallel with scrambled shRNA control.

2023-07-12 | E-MTAB-11570 | biostudies-arrayexpress

Methyltransferase-like 3 (METTL3) regulates exocytosis

Project description:RNA modification pathways are often mis-regulated in various typers of cancer, with N6-methyladenosine (m6A) playing a pivotal role in cancer progression and metastasis. Methyltransferase-like 3 (METTL3), a core component of the m6A methyltransferase complex, functions not only as an m6A writer but also promotes tumorigenesis through m6A-independent mechanisms. Here, we show that METTL3 is mislocalized to the cytoplasm in breast cancer tumors from patients, contributing to the oncogenic phenotype. Cytoplasmic METTL3 interacts with EXOC7, a key exocytosis regulator. Additionally, METTL3 regulates m6A-dependent alternative splicing (AS) of EXOC7, promoting the expression of a more aggressive isoform. Silencing METTL3 impairs vesicle trafficking and alters the breast cancer secretome. These effects arenot dependent on its enzymatic activity but instead associated with METTL3-mediated stabilization of EXOC7. Furthermore, knockdown of METTL3 , but not inhibition of its catalytic function, impairs invadopodia formation, collagen matrix invasion, and the generation of focal adhesions , all of which are critical for extracellular matrix degradation and cell invasion. Our findings uncover non-catalytic roles of METTL3 in regulating exocytosis and the cancer secretome, with broader implications for other cancer types.

2026-05-04 | PXD066045 | Pride

METTL3 promotes translation in human cancer cells

Project description:we find METTL3 associates with polyribosomes and promotes translation. METTL3 depletion inhibits translation, and both wild-type and catalytically inactive METTL3 promote translation when tethered to the 3' untranslated region (UTR) of a reporter mRNA. Mechanistically, METTL3 enhances mRNA translation through an interaction with the translation initiation machinery. m6A seq in A549 and H1299 cells, RNA seq in METTL3 knockdown cells

2016-07-03 | E-GEOD-76367 | biostudies-arrayexpress

Mass spectrometry analysis of METTL3 phosphorylation in extracellular growth factor signaling

Project description:A fundamental facet of cell signaling is the conversion of extracellular signals into adaptive transcriptional responses. The role of RNA modifications in this process is poorly understood. We found that epidermal growth factor (EGF) promotes ERK-dependent phosphorylation of the m6A writer enzyme METTL3 at serine-43. Serine-43 phosphorylation increased METTL3-mediated methylation of the small nuclear RNA 7SK. Here we performed of phosphorylation mass spectrometry based on Data independent acquisition (DIA) of Hela cells stimulated with EGF in the absence or presence of the inhibitor U0126. Additionally, we validated known interactions between the 7SK-associated protein LARP7. Our findings establish a novel function for the m6A modification in converting growth-factor signaling events to a transcriptional elongation regulatory response via an RNA-methylation-dependent switch mediated by ERK signaling.

2023-06-27 | PXD036344 | Pride

METTL3 KD in HepG2 cells

Project description:To gain insight into possible processes that require m6A for their function, METTL3 was knocked down (KD) in HepG2 cells by siRNA transfections Differential expression analysis of METTL3 KD versus mock-transfected HepG2 cells, in 2 biological replicates

2012-04-25 | E-GEOD-37001 | biostudies-arrayexpress

m6A-RIP-seq of mRNA in yw, Mettl3, Mettl14 and Hakai flies

Project description:In order to obtain a stringent m6A methylome in Drosophila adults, we performed m6A-RIP-seq in yw control (male and female), Mettl3 (male), Mettl14 (male) and Hakai (male) mutant flies. We find that the effective m6A modification, which depends on the writer complex, is mostly distributed in 5’ UTR and near start codon in Drosophila, in contrast to the mammalian system. We define a set of high-confident m6A methylation sites shared by Mettl3, Mettl14 and Hakai, indicating that Hakai is a core component of the m6A writer complex. We also find differential methylation pattern in certain loci between male and female flies.

2021-03-01 | GSE155662 | GEO

Binding motif analysis of METTL3，WTAP in METTL3，WTAP overexpressed Human 293T cells

Project description:label the cells overexpressed Myc tagged METTL3 and Flag tagged WTAP with 4-SU, the RNA bound by METT3,WTAP can be got by Myc or Flag IP followed by RNA isolation by using the TRIzol (Invitrogen) reagent by following the company manual.the RNA was then used for library preparation using a TruSeq™ RNA Sample Prep Kit v2 (Illumina, San Diego, CA, USA) according to the manufacturer’s protocol.The libraries were sequenced using HiSeq2000 (Illumina) in single-read mode, creating reads with a length of 50 bp. Sequencing chemistry v2 (Illumina) was used and samples were multiplexed in two samples per lane. discovery of the binding motif of METTL3，WTAP in METTL3，WTAP overexpressed Human 293T cells

2014-01-16 | E-GEOD-50580 | biostudies-arrayexpress

RNA N6-methyladenosine modulates endothelial atherogenic responses to disturbed flow in mice

Project description:Atherosclerosis preferentially occurs in atheroprone vasculature where human umbilical vein endothelial cells (HUVECs) are exposed to disturbed flow. Disturbed flow is associated with vascular inflammation and focal distribution. Recent studies have revealed the involvement of epigenetic regulation in atherosclerosis progression. N6-methyladenosine (m6A) is the most prevalent internal modiﬁcation of eukaryotic mRNA, but its function in endothelial atherogenic progression remains unclear. Here, we show that m6A mediates the EGFR signaling pathway during EC activation to regulate the atherosclerotic process. Oscillatory stress (OS) reduced the expression of METTL3, the primary m6A methyltransferase. Through m6A sequencing and functional studies, we determined that m6A mediates the mRNA decay of the vascular pathophysiology gene EGFR which leads to EC dysfunction. m6A modification of the EGFR 3’UTR accelerated its mRNA degradation. Double mutation of the EGFR 3’UTR abolished METTL3-induced luciferase activity. Adenovirus-mediated METTL3 overexpression significantly reduced EGFR activation and endothelial dysfunction in the presence of OS. Furthermore, TSP-1, an EGFR ligand, was specifically expressed in atheroprone regions without being affected by METTL3. Inhibition of the TSP-1/EGFR axis by using shRNA and AG1478 significantly ameliorated atherogenesis. Overall, our study revealed that METTL3 alleviates endothelial atherogenic progression through m6A-dependent stabilization of EGFR mRNA, highlighting the important role of RNA transcriptomics in atherosclerosis regulation.

2025-06-20 | GSE299805 | GEO

METTL3 alters capping enzyme expression and its activity on ribosomal proteins in NSCLC cell model

Project description:The 5’ cap, catalyzed by capping enzyme, RNGTT, is a vital mRNA modification for the functionality of mRNAs and dysregulated in cancer cells. The m6A writer METTL3 is a regulator of mRNA stability and protein translation, and its expression is altered in various cancers, including lung cancer cells. We identified a METTL3 motif in the mRNA of RNGTT and investigated whether METTL3 could regulate the expression of RNGTT. Knock down of METTL3 resulted in destabilizing RNGTT mRNA, reduced protein expression and activity. Sequencing of capped mRNAs and m7G immunoprecipitation identified an underrepresentation of ribosomal protein mRNA.

2024-10-21 | GSE273305 | GEO

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