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METTL16 promotes translation and lung tumorigenesis by sequestering cytoplasmic eIF4E2

ABSTRACT: METTL16 promotes translation and lung tumorigenesis by sequestering cytoplasmic eIF4E2

PROVIDER: PRJNA812878 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18220805_1.fastq.gz	Fastqsanger.gz
	SRR18220805_2.fastq.gz	Fastqsanger.gz
	SRR18220806_1.fastq.gz	Fastqsanger.gz
	SRR18220806_2.fastq.gz	Fastqsanger.gz
	SRR18220807_1.fastq.gz	Fastqsanger.gz

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METTL16 promotes translation and lung tumorigenesis by sequestering cytoplasmic eIF4E2

Project description:METTL16 was previously identified as an m6A methyltransferase. In this study, we validated the cytoplasmic location of METTL16 and explored its function in the cytoplasm. We found that METTL16 promoted translation by sequestering eIF4E2, a translation initiation repressor, from the 5' cap structure.

2022-03-07 | GSE197915 | GEO

Identifying interaction proteins of METTL16 using co immunoprecipitation and mass spectroscopy

Project description:METTL16 has recently been identified as an RNA methyltransferase that installs m6A marks on a few transcripts. But its function in cytosol remains unclear. Puromycin-labelling and renilla luciferase assay revealed that METTL16 can promote translation efficiency in an m6A-independent manner. To explore the mechanism, we performed co-immunoprecipitation using METTL16 antibody and mass spectroscopy to identify its interaction proteins. Moreover, we find that METTL16 is essential for tumorigenesis of non-small cell lung cancer.

2024-08-03 | PXD032068 | Pride

Determine the effects of METTL16 on global translation efficiency via ribosome profiling (Ribo-seq)

Project description:METTL16 is a member of methyltransferase like (METTL) family. Unlike well-studied METTL3 and METTL14, we found a much higher percentage of METTL16 is localized in the cytosol. The subcellular distribution holds the ability to potentiate translation efficiency. Via Far-western blotting and Co-Immunoprecipitation (Co-IP) assays, we have identified the direct interactions between METTL16 and eukaryotic initiation factor 3 (eIF3) a and b. Via cross-linking immunoprecipitation and qPCR (CLIP-qPCR), we have discovered the direct associations between METTL16 and rRNAs. The METTL16-eIF3a/b and METTL16-rRNAs interactions induce the binding between eIF3 and 18S rRNA, promote the formation of 43S preinitiation complex, and eventually expedite translation initiation, the rate-limiting step of translation. To determine the exact effects of METTL16 on translation efficiency, we performed ribosome profiling (Ribo-seq) with HEK293T upon CRISPR-Cas9-induced METTL16 knockout. To guarantee the repeatability and avoid any potential off-target effects, we included 3 distint sgRNAs against METTL16.

2021-10-28 | GSE156796 | GEO

METTL16 deficiency attenuates apoptosis through translational control of extrinsic death receptor during nutrient deprivation

Project description:METTL16 is a well-characterized m6A methyltransferase that has been reported to contribute to tumorigenesis in various types of cancer. However, the effect of METTL16 on tumor progression under restricted nutrient conditions, which commonly occur in tumor microenvironment, has yet to be elucidated. Herein, our study initially reported the inhibitory effect of METTL16 depletion on apoptosis under amino acid starvation conditions.

2023-11-11 | GSE244901 | GEO

METTL16 deficiency attenuates apoptosis through translational control of extrinsic death receptor during nutrient deprivation

2024-03-01 | GSE249176 | GEO

RNA-seq in wild-type, METTL16-knockout, and METTL16 rescue NOMO-1 cells

Project description:METTL16 belongs to methyltransferase like (METTL) family and could install m6A marks on its substrates. Here, we uncover a tumor-promoting role of METTL16 in AML and LSC self-renewal. To explore the mechanism underlying the oncogenic function of METTL16 in AML, we performed m6A-seq and RNA-seq. Via integrated analysis of m6A-seq data and RNA-seq data, we identified two bona fide targets of METTL16, BCAT1 and BCAT2. METTL16 functions as an m6A methyltransferase to regulate expression of BCAT1 and BCAT2, which contribute to reprogramming BCAA metabolism.

2023-01-12 | GSE190044 | GEO

Determine the methyltransferase activities of METTL16 via MeRIP-seq (m6A-seq)

2023-01-12 | GSE189995 | GEO

RNA Methyltransferase METTL16's Protein Domains Have Differential Functional Effects on Cell Processes

Project description:To investigate the cellular role of METTL16, we established HEK293 cell lines over expressing wild-type METTL16 or METTL16 methylation and RNA binding mutations. We then removed endogenous METTL16 from the cells using CRISPR. We then performed gene expression profiling analysis using data obtained from RNA-seq of the various cell lines.

2023-06-29 | GSE217192 | GEO

RNA-seq analysis after siRNA-METTL16 treatment in PANC-1 cells

Project description:RNA-seq analysis was performed in PDAC patient-derived cell line PANC-1 (NC and METTL16-silenced) to analyze the expression of RNA levels after loss of METTL16.

2023-04-18 | GSE226518 | GEO

Mettl16 promotes hematopoietic stem and progenitor cell expansion in embryonic hematopoiesis [m6A-Seq]

Project description:The RNA N6-methyladenosine (m6A) modification has emerged as an essential regulator of vertebrate embryogenesis and malignancies. However, its functions and underlying molecular mechanisms in the expansion of hematopoietic stem and progenitor cells (HSPCs) during early embryonic development remain elusive. Here we show that Mettl16, an RNA methyltransferase identified recently, is specifically required for HSPC expansion during zebrafish early embryonic development in an m6A-dependent manner. In mettl16 deficient embryos, HSPCs exhibit defective proliferation capacity due to G0/G1 arrest. Mechanistically, HSPC proliferation is blocked by impaired methyltransferase function of Mettl16 in vivo. We identify cell cycle gene mybl2b as a novel direct m6A target of Mettl16, and Mettl16 deficiency destabilizes mybl2b mRNA, which is mediated by m6A reader Igf2bp1. Moreover, we revealed that the METTL16-m6A-MYBL2-IGF2BP1 signaling axis in G1/S progression is conserved in humans. Collectively, our findings demonstrate the critical function of m6A modification deposited by Mettl16 in HSPC expansion during early embryonic development.

2024-03-04 | GSE225136 | GEO

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