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Identification of m6A-modified YTHDF2 targets by high-throughput m6A-seq and RIP-seq in HBV-infected HepG2 cells

ABSTRACT: Identification of m6A-modified YTHDF2 targets by high-throughput m6A-seq and RIP-seq in HBV-infected HepG2 cells

PROVIDER: PRJNA823764 | ENA |

REPOSITORIES: ENA

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Identification of m6A-modified YTHDF2 targets by high-throughput m6A-seq and RIP-seq in HBV-infected HepG2 cells [RIP-seq]

Project description:We investigated the role of O-GlcNAcylation of m6A reader YTHDF2 in HBV-related hepatocarcinogenesis and progression. We found that YTHDF2 O-GlcNAcylation was elevated upon HBV infection through upregulated HBP. OGT-mediated YTHDF2 O-GlcNAcylation at Ser263 enhanced its protein stability, and subsequently changed the gene expression profiles. Mechanistically, we identified YTHDF2 stabilized minichromosome maintenance protein 2 (MCM2) and MCM5 mRNAs in an m6A dependent manner by high-throughput profiling of m6A-seq and RIP-seq, thereby promoting HBV-related HCC tumorigenesis. Importantly, our study proposed that targeting OGT-mediated YTHDF2 O-GlcNAcylation may be a novel strategy for potential treatment of HBV-associated liver cancer.

2023-02-15 | GSE200259 | GEO

Identification of m6A-modified YTHDF2 targets by high-throughput m6A-seq and RIP-seq in HBV-infected HepG2 cells [m6A-seq]

2023-02-15 | GSE200260 | GEO

Identification of m6A-modified YTHDF2 targets by high-throughput m6A-seq and RIP-seq in HBV-infected HepG2 cells [m6A-seq]

Project description:Identification of m6A-modified YTHDF2 targets by high-throughput m6A-seq and RIP-seq in HBV-infected HepG2 cells [m6A-seq]

| PRJNA823805 | ENA

Identification of m6A-modified YTHDF2 targets by high-throughput m6A-seq and RIP-seq in HBV-infected HepG2 cells [RIP-seq]

Project description:Identification of m6A-modified YTHDF2 targets by high-throughput m6A-seq and RIP-seq in HBV-infected HepG2 cells [RIP-seq]

| PRJNA823804 | ENA

The RNA m6A reader YTHDF2 maintains oncogene expression and is a targetable dependency in glioblastoma stem cells [m6A RIP-seq]

Project description:Glioblastoma is a universally lethal cancer driven by glioblastoma stem cells (GSCs). Here, we interrogated N6-methyladenosine (m6A) mRNA modifications in GSCs by methyl RNA-immunoprecipitation followed by sequencing (meRIP-seq) and transcriptome analysis, finding transcripts marked by m6A often upregulated. Interrogating m6A regulators, GSCs displayed preferential expression as well as in vitro and in vivo dependency of the m6A reader, YTHDF2, in contrast to normal neural stem cells (NSCs). While YTHDF2 has been reported to destabilize mRNAs, YTHDF2 stabilized the oncogene transcripts, MYC and VEGFA, in GSCs in an m6A-dependent manner. We identified IGFBP3 as a downstream effector of the YTHDF2-MYC axis in GSCs and IGF1/IGF1R inhibitor, Linsitinib, as preferentially targeting YTHDF2-expressing cells, inhibiting the viability of GSCs without affecting NSCs and impairing in vivo glioblastoma growth. Thus, YTHDF2 links RNA epitranscriptomic modifications and GSC growth, laying the foundation for the YTHDF2-MYC-IGFBP3 axis as a specific and novel therapeutic target in glioblastoma.

2020-09-29 | GSE158741 | GEO

m6A-dependent regulation of messenger RNA stability

Project description:N6-methyladenosine (m6A) is the most prevalent internal modification present in the mRNA of all higher eukaryotes. Here we present that m6A is selectively recognized by human YTH domain family (YTHDF2) protein to regulate mRNA degradation. By using crosslinking and immunoprecipitation, we have identified over 4000 substrate RNA of YTHDF2 with conserved core motif of G(m6A)C. We further estabilshed the role of YTHDF2 in RNA metabolism by a combination of ribosome profiling, RNA sequencing, m6A level quantification and cell-based imaging: the C-terminal domain of YTHDF2 selectively binds to m6A of mRNA and the N-terminal domain is responsive for localizing mRNA from translatable pool to processing body where mRNA decay occurs. PAR-CLIP and RIP was used to identify YTHDF2 binding sites followed by ribosome profling and RNA seq to assess the consequences of YTHDF2 siRNA knock-down

2013-11-29 | E-GEOD-49339 | biostudies-arrayexpress

YTHDF2 mediates the mRNA degradation in prostate cancer in m6A-dependent way

Project description:As the crucial m6A reader, YTHDF2 usually degrades the target mRNAs by recognizing the m6A modified sites, consequently altering m6A levels of each mRNA. In this study, we used m6A MeRIP sequencing to detect the m6A modification alterations in prostate cancer (PCa) cell line after knocking down YTHDF2 and identify how YTHDF2 promote the PCa progression by mediating the mRNA degradation in m6A-dependent way.

2020-11-09 | GSE129408 | GEO

YTHDF2-m6A-NF-kB axis controls anti-tumor immunity through regulating intratumoral Treg survival and function [RIP-seq]

Project description:N6-methyladenosine (m6A) in messenger RNA (mRNA) regulates immune cells in homeostasis and in response to infection and inflammation. The function of YTHDF2 in the tumor microenvironment (TME) in these contexts has not been explored. We discovered that loss of Ythdf2 in regulatory T (Treg) cells can reduce tumor growth in mice while maintaining peripheral homeostasis. In the tumor microenvironment, Ythdf2-deficient Treg cells have impaired function and poor survival. The elevated tumor necrosis factor (TNF) signaling in the TME grants the location-specific function of YTHDF2, which participates in the feedback regulation of NF-kB signaling by accelerating the degradation of m6A-modified, NF-kB negative regulators, Nlrc3, Nfkbie, and Traf3. TME-specific regulation of Treg by YTHDF2 points to YTHDF2 as a target for anti-cancer immunotherapy, where intratumoral Treg cells can be targeted to enhance antitumor immune response, while avoiding Treg cells in the periphery to minimize undesired inflammations.

2023-06-07 | GSE216958 | GEO

Ythdf2-mediated m6A mRNA clearance modulates neural development in mice

Project description:We found that the proliferation and differentiation capabilities of NSPCs decrease significantly in Ythdf2 null mutants.To explore the underlying molecular mechanism, we performed transcriptomics and well-established m6A-methylome analyses of NSPCs dervied from wild type and Ythdf2-/- embryo brains. RNA-seq data revealed that expressions of genes enriched in neural development pathways were significantly disturbed. The inhibitory genes, like Flrt2, Ptprd, et al. in regulation of JAK-STAT cascade, which contributes to the neuroprotection and neurite outgrowth, showed increased gene expressions and m6A enrichment by m6A-seq. We identified that without the recognizing and binding of Ythdf2, the degradation of neuron differentiation related m6A-modified mRNAs were delayed in Ythdf2-/-, thereby disturbing the proliferation and differentiation of NSPCs. In summary, our findings uncovered that Ythdf2 modulates neural developmental via regulating the clearance of mRNA targets.

2018-01-01 | GSE104867 | GEO

m6A meRIP-Seq from Ythdf2CTL pre-leukemic cells

Project description:The mRNA m6A reader YTHDF2 is overexpressed in a broad spectrum of human acute myeloid leukemias (AML). To understand the role of YTHDF2 in AML, we generated m6A meRIP-seq libraries form Ythdf2fl/fl (Ythdf2CTL) pre-leukemic cells.

2019-04-05 | E-MTAB-6791 | biostudies-arrayexpress

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