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Clinical and molecular significance of the RNA m6A methyltransferase complex in prostate cancer

ABSTRACT: shRNAs targeting METTL3 used to deplete METTL3 in castrate-resistant LNCaP:C42 prostate cancer cells and the effect on gene expression and splicing determined.

ORGANISM(S): Homo sapiens

PROVIDER: GSE210130 | GEO | 2023/01/04

REPOSITORIES: GEO

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The METTL3 RNA methyltransferase regulates androgen signalling in castrate resistant prostate cancer cells

Project description:iRNAs targeting METTL3 used to deplete METTL3 in castrate resistant LNCaP:C42 and 22Rv1 prosate cancer cells and the effect on basal and androgen regulated gene expression and splicing determined.

2022-11-02 | GSE194420 | GEO

Exploring the Impact of m6A Methyltransferase Mettl3 on MASLD through Multi-Omics Analysis

Project description:Background: N6-methyladenosine (m6A) RNA modification plays a crucial role in various biological events and is implicated in various metabolic-related diseases. However, its role in MASLD remains unclear. This study aims to investigate the impact of Mettl3 on MASLD through multi-omics analysis, with a focus on exploring its potential mechanisms of action. Methods: MASLD mouse models were established by feeding a high-fat diet for 12 weeks, and Mettl3 stable overexpression AML12 cell models were constructed via lentiviral transfection. Subsequent transcriptomic and proteomic analyses, as well as integrated analysis between different omics datasets, were conducted. Results: Mettl3 expression significantly increased in MASLD mouse models. In the transcriptomic and proteomic analyses, we identified 848 genes with significant inconsistencies between transcriptomic and proteomic datasets. GO/KEGG enrichment terms may involve post-transcriptional modifications, particularly Mettl3-mediated m6A modification. Subsequently, through integrated proteomic analysis of Mettl3-overexpressed AML12 cell models and MASLD mouse models, we selected the top 20 co-upregulated and co-downregulated GO/KEGG terms as the main biological processes influenced by Mettl3 in MASLD. By intersecting with pathways obtained from previous integrated analyses, we identified GO/KEGG terms affected by Mettl3-induced m6A modification. Protein-protein interaction analysis of proteins involved in these pathways highlighted GAPDH, ENO1, and TPI1 as three key hub genes. Conclusion: In MASLD, Mettl3 regulates the glycolytic pathway through m6A modification, influencing the occurrence and development of the disease via the key hub genes GAPDH, ENO1, and TPI1. These findings expand our understanding of MASLD and provide strong evidence for potential therapeutic targets and drug development.

2024-09-20 | PXD050565 | Pride

A Cleavage Product METTL3a-(238-580) Mediates m6A Methyltransferase Complex Assembly and mTOR Activation

Project description:N6-methyladenosine (m6A) methylation of mRNA by the methyltransferase complex (MTC), with core components including METTL3-METTL14 heterodimers and Wilms’ tumor 1-associated protein (WTAP), contributes to breast tumorigenesis, but the mechanism of MTC assembly remains elusive. Here, we identify a novel cleaved form METTL3a (residues 239-580 of METTL3), that is highly expressed in breast cancer. Furthermore, we find that both METTL3a and full-length METTL3 are required for MTC assembly, RNA m6A deposition, as well as cancer cell proliferation. Mechanistically, we find that METTL3a is required for METTL3-METTL3 interaction, which is a prerequisite step for recruitment of WTAP in MTC assembly. Analysis of m6A sequencing data shows that depletion of METTL3a globally disrupts m6A methylation, and METTL3a mediates mTOR activation via m6A-mediated suppression of TMEM127 expression. Consequently, we find that METTL3 cleavage is mediated by proteasome in an mTOR-dependent manner, revealing positive regulatory feedback between METTL3a and mTOR signaling. Our findings reveal METTL3a as an important component for MTC assembly, and suggest the METTL3a-mTOR axis as a potential therapeutic target for breast cancer.

2023-08-16 | GSE213727 | GEO

m6A-seq profiling in Mettl3 Ctrl and dTAG13 mESCs [m6Aseq]

Project description:dTAG-13 treated METTL3_FKBP12(F36V) is sufficient to functionally deplete m6A methylation, that catalysed by METTL3/14 complex.

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The METTL3 RNA methyltransferase regulates gene expression in castrate resistant LNCaP:C42 prostate cancer cells

Project description:The METTL3 RNA methyltransferase regulates gene expression in castrate resistant LNCaP:C42 prostate cancer cells

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The m6A methyltransferase Mettl3 deficiency attenuates hepatic stellate cell activation and liver fibrosis [m6A-RIP-seq]

Project description:m6A-RIP sequencing of primary hepatic stellate cells (HSCs) isolated from Control and HSC-specific Mettl3-knockout (Mettl3 cKO) mouse liver tissues.

2022-07-13 | GSE207908 | GEO

Clinical and molecular significance of the RNA m6A methyltransferase complex in prostate cancer

Project description:Clinical and molecular significance of the RNA m6A methyltransferase complex in prostate cancer

| PRJNA863879 | ENA

Proteomic analysis of castrate resistant prostate cancer cell lines

Project description:In this study the development of androgen independence in a cell model of disease was selected as a mirror of to the events at play in the development of Castrate Resistant Prostate Cancer in-vivo. LNCaP cells which are androgen dependent and androgen independent sublines; LNCaP-Abl and LNCaP-Abl-Hof were subject to extensive fractionation by 1-D SDS PAGE and accurate mass-high resolution mass spectrometry (Q Exactive) to identify proteins whose expression was changes significantly in response to androgen independent growth.

2022-02-28 | PXD000751 | Pride

BET inhibition abrogates global transcription via repressing m6A writer complex

Project description:To characterize the role of m6A modification in mediating BRD4-dependent biological functions, we established METTL3 reconstituting cells and treated with JQ1 BRD4 directs gene transcription through diverse mechanisms. Here, we specifically focused on BETi-dependent transcriptome or chestrated by m6A-mediated regulation. To this end, we first need to identify bona fide m6A-dependent transcripts via rescue experiments in METTL3-knockdown cells by adding back wild-type METTL3 or METTL3-CD mutant (a catalytically inactive form of METTL3)

2023-12-31 | GSE219191 | GEO

Redox Regulation of m6A Methyltransferase METTL3 in Human Beta Cells Controls the Innate Immune Response in Type 1 Diabetes

Project description:Label-free proteomics of S-nitrosylation on recombinant human METTL3 induced by S-Nitroso-N-acetyl-DL-penicillamine (SNAP) to determine redox-sensitive Cys sites

2023-03-24 | MSV000091547 | MassIVE

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