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METTL3 preferentially enhances non-m6A translation of epigenetic factors and promotes tumorigenesis (meRIP, RIP and polysome-seq)

ABSTRACT: METTL3 preferentially enhances non-m6A translation of epigenetic factors and promotes tumorigenesis (meRIP, RIP and polysome-seq)

PROVIDER: PRJNA685739 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13259132_1.fastq.gz	Fastqsanger.gz
	SRR13259132_2.fastq.gz	Fastqsanger.gz
	SRR13259133_1.fastq.gz	Fastqsanger.gz
	SRR13259133_2.fastq.gz	Fastqsanger.gz
	SRR13259134_1.fastq.gz	Fastqsanger.gz

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METTL3 preferentially enhances non-m6A translation of epigenetic factors and promotes tumorigenesis (meRIP, RIP and polysome-seq)

Project description:Methyltransferase-like 3 (METTL3) is the best known m6A methyltransferase of the N6-adenosine-methyltransferase complex that functions in the reversible epi-transcriptome modulation of m6A modification. Besides acting as a m6A methyltransferase, METTL3 also regulates mRNA translation as well as other biological processes either through m6A “reader”-mediated downstream effect or directly binding to m6A sites, but the underlying mechanism and biological significance of these cytoplasmic events remain undefined. Here, we demonstrated that METTL3 inhibition significantly delayed gastric tumorigenesis in patient-derived xenograft model. Intriguingly, global METTL3-binding profiling revealed METTL3 occupied numerous oncogenic mRNAs without m6A signals, indicating a novel mechanism independent of m6A machinery. Furthermore, METTL3 was observed to translocate from nucleus to cytoplasm during gastric carcinogenesis, and its cytoplasm-to-nucleus ratio was correlated with cancer progression. In addition, the nuclear retention of METTL3 nearly abolished its tumor-promoting activity. Mechanistically, METTL3 interacted with PABPC1 to promote RNA looping, thus facilitating the translation of multiple oncogenic mRNAs. Taken together, our findings indicate an unexpected role of METTL3 as an important translational regulator independent of either m6A-“writer” or -“reader” activities and suggest METTL3 as a therapeutic target in gastric cancer.

2022-05-16 | GSE163310 | GEO

Mettl3-RIP-sequencing and m6A-MeRIP-sequencing of NK cells

Project description:Mettl3-RIP-sequencing and m6A-MeRIP-sequencing of NK cells

| PRJNA725178 | ENA

METTL3-dependent m6A modification programs human neural progenitor cell proliferation [MeRIP-seq]

Project description:To investigate whether the role of METTL3 in hNPCs is dependent on its m6A activity,samples form neural progenitor cell (NPC) differentiation in the small molecule-assisted shut-off (SMASh) tagged hESC groups were collected. Gene expression levels were quantitated by RNA-seq analysis, and the potential target genes were identified by MeRIP-seq analysis and RIP-seq.

2023-11-22 | GSE242519 | GEO

METTL3-dependent m6A modification programs human neural progenitor cell proliferation [RIP-seq]

2023-11-22 | GSE242520 | GEO

MeRIP-seq to explore the targets of METTL3 in pancreatic cancer

Project description:We performed MeRIP-seq of METTL3-knockdown (KD) MIAPaCa-2 and control cells to detect METTL3-methylated genes and extracted genes whose methylation was lost in METTL3-KD cells compared with control cells. Next, we performed mRNA expression analysis using dates of input samples at MeRIP-seq. Genes whose methylation peaks were abolished by METTL3-KD and whose expression changes were observed were analyzed as candidates for METTL3-regulated genes.

2021-12-13 | GSE190078 | GEO

MeRIP-sequencing data from H1975 cells with NC or METTL3-sh

Project description:We use MeRIP-sequencing to evaluate the effect of METTL3 knockdown on the gene changes in H1975 cells.

2020-12-07 | GSE147171 | GEO

MeRIP-Seq (m6A-Seq) identifies the mRNA m6A modification target in negative control and METTL3 knockdwon HULEC-5a

Project description:To identify the molecular mechanism by which METTL3 regulates endothelial barrier function, we performed RNA-seq and MeRIP-seq in HULEC-5a cells with stable METTL3 knockdown and control cells. The RNA-seq results revealed that 437 transcripts were significantly downregulated (fold change <0.5) after METTL3 knockdown. The MeRIP-seq results revealed that the m6A peaks in 1011 transcripts were decreased in abundance (fold change >1.2). Intriguingly, 55 transcripts overlapped in the RNA-seq and MeRIP-seq data

2022-05-20 | GSE200648 | GEO

Mettl3-RIP-sequencing of NK cells

Project description:Mettl3-RIP-sequencing of NK cells

| PRJNA725188 | ENA

Mettl3-RIP-sequencing of NK cells

Project description:m6A modification plays vital roles in regulating mRNA lifecycle, thus controlling the biological process of multiple cell types. Here we intended to discover the binding sites of Mettl3 protein on mRNA of NK cells. Total RNAs were isolated from WT splenic NK cells, and subjected to standard RIP protocol. The library products corresponding to 200-500 bps were enriched, quantified and finally sequenced on Illumina Novaseq 6000 sequencer with PE150 model. Mettl3 binding sites were located primarily in the 3’ untranslated regions (UTRs), coding sequences (CDSs) region and near stop codons.

2021-07-20 | GSE173325 | GEO

METTL3 mediated m6A mRNA methylation regulates neutrophil activation through targeting TLR4 signaling (meRIP-Seq)

Project description:To investigate the effect of METTL3 function in the regulation of neutrophil activation, we established neutrophil METTL3 knock out mice by crossing METTL3flox/flox mice with Lyzm-cre mice. We then performed gene expression profiling analysis using data obtained from MeRIP-seq of isolated neutrophil from METTL3f/f and METTL3f/f Lyzm-Cre mice .

2023-03-31 | GSE225139 | GEO

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