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CRTC2 Forms Co-condensates with YTHDF2 that Enhance Translational Efficiency of m6A-Modified mRNAs to Drive Hepatocarcinogenesis and Lenvatinib Resistance (m6A-seq)

ABSTRACT: CRTC2 Forms Co-condensates with YTHDF2 that Enhance Translational Efficiency of m6A-Modified mRNAs to Drive Hepatocarcinogenesis and Lenvatinib Resistance (m6A-seq)

PROVIDER: PRJNA1101528 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28724279_1.fastq.gz	Fastqsanger.gz
	SRR28724279_2.fastq.gz	Fastqsanger.gz
	SRR28724280_1.fastq.gz	Fastqsanger.gz
	SRR28724280_2.fastq.gz	Fastqsanger.gz

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CRTC2 Forms Co-condensates with YTHDF2 that Enhance Translational Efficiency of m6A-Modified mRNAs to Drive Hepatocarcinogenesis and Lenvatinib Resistance (CRTC2-RIPseq)

Project description:As the third most common cause of cancer-related mortality, hepatocellular carcinoma (HCC) is a global health concern. Despite its prevalence, treatment options are limited, underscoring the need to identify potential therapeutic targets and strategies. Here, we identified amplification of CRTC2, situated in the 1q21.3 region, due to copy number alterations in HCC. In a cohort of patients with HCC, CRTC2 protein levels were frequently elevated and correlated with poor prognosis. Genetic depletion of CRTC2 significantly impeded the onset and progression of HCC in mouse models. CRTC2 formed cytoplasmic condensates that recruited the m6A reader YTHDF2. Furthermore, CRTC2 promoted the translocation of m6A-modified mRNAs from decay sites to polyribosomes by interacting with PABP1. The activities of CRTC2 counteracted YTHDF2-mediated mRNA degradation to enhance the translational efficiency of specific mRNAs, including those encoding LRP5 and c-Jun. Targeting CRTC2 in hepatocytes using AAV8.sgCRTC2 elicited substantial therapeutic benefits in HCC mouse model and significantly enhanced the sensitivity to lenvatinib. Together, this research elucidates the pivotal role and underlying molecular mechanisms of CRTC2 in hepatocarcinogenesis and lenvatinib-resistance, highlighting its potential clinical and therapeutic applications.

2025-02-08 | GSE264239 | GEO

CRTC2 Forms Co-condensates with YTHDF2 that Enhance Translational Efficiency of m6A-Modified mRNAs to Drive Hepatocarcinogenesis and Lenvatinib Resistance (m6A-seq)

2025-02-08 | GSE264244 | GEO

CRTC2 Forms Co-condensates with YTHDF2 that Enhance Translational Efficiency of m6A-Modified mRNAs to Drive Hepatocarcinogenesis and Lenvatinib Resistance (RNA-seq)

2025-02-10 | GSE289166 | GEO

CRTC2 Forms Co-condensates with YTHDF2 that Enhance Translational Efficiency of m6A-Modified mRNAs to Drive Hepatocarcinogenesis and Lenvatinib Resistance (YTHDF2-RIPseq)

2025-02-08 | GSE264246 | GEO

CRTC2 Forms Co-condensates with YTHDF2 that Enhance Translational Efficiency of m6A-Modified mRNAs to Drive Hepatocarcinogenesis and Lenvatinib Resistance (CRTC2-RIPseq)

Project description:CRTC2 Forms Co-condensates with YTHDF2 that Enhance Translational Efficiency of m6A-Modified mRNAs to Drive Hepatocarcinogenesis and Lenvatinib Resistance (CRTC2-RIPseq)

| PRJNA1101517 | ENA

CRTC2 Forms Co-condensates with YTHDF2 that Enhance Translational Efficiency of m6A-Modified mRNAs to Drive Hepatocarcinogenesis and Lenvatinib Resistance (YTHDF2-RIPseq)

Project description:CRTC2 Forms Co-condensates with YTHDF2 that Enhance Translational Efficiency of m6A-Modified mRNAs to Drive Hepatocarcinogenesis and Lenvatinib Resistance (YTHDF2-RIPseq)

| PRJNA1101539 | ENA

CRTC2 Forms Co-condensates with YTHDF2 that Enhance Translational Efficiency of m6A-Modified mRNAs to Drive Hepatocarcinogenesis and Lenvatinib Resistance (RNA-seq)

Project description:CRTC2 Forms Co-condensates with YTHDF2 that Enhance Translational Efficiency of m6A-Modified mRNAs to Drive Hepatocarcinogenesis and Lenvatinib Resistance (RNA-seq)

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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

Identification of m6A-modified YTHDF2 targets by high-throughput m6A-seq and RIP-seq in HBV-infected HepG2 cells [m6A-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 | GSE200260 | 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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