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YTHDF3 Induces the Translation of m6A-enriched Metastasis-associated Gene Transcripts to Promote Breast Cancer Brain Metastasis [m6A-seq]

ABSTRACT: YTHDF3 Induces the Translation of m6A-enriched Metastasis-associated Gene Transcripts to Promote Breast Cancer Brain Metastasis [m6A-seq]

PROVIDER: PRJNA534214 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8944231.fastq.gz	Fastqsanger.gz
	SRR8944232.fastq.gz	Fastqsanger.gz
	SRR8944233.fastq.gz	Fastqsanger.gz
	SRR8944234.fastq.gz	Fastqsanger.gz

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Similar Datasets

YTHDF3 Induces the Translation of m6A-enriched Metastasis-associated Gene Transcripts to Promote Breast Cancer Brain Metastasis [m6A-seq]

Project description:Brain metastasis is a major cause of cancer mortality, but its molecular mechanisms are severely understudied. We found that YTHDF3 overexpression clinically correlates with brain metastases in breast cancer patients and is required for brain metastasis. Silencing YTHDF3 suppressed the brain metastasis of breast cancer cells in vitro and in vivo. Integrated transcriptome and m6A-seq analysis revealed alter expression of selected YTHDF3 target genes, including ST6GALNAC5, GJA1, and EGFR by promoting m6A-dependent translation of these target transcripts. Our work uncovers an essential role of YTHDF3 in controlling the interaction between cancer cells and brain microenvironment, thereby gaining brain metastatic competence.

2020-09-30 | GSE130172 | GEO

YTHDF3 Induces the Translation of m6A-enriched Metastasis-associated Gene Transcripts to Promote Breast Cancer Brain Metastasis [RIP-Seq]

2020-09-30 | GSE130171 | GEO

YTHDF3 Induces the Translation of m6A-enriched Metastasis-associated Gene Transcripts to Promote Breast Cancer Brain Metastasis

Project description:YTHDF3 Induces the Translation of m6A-enriched Metastasis-associated Gene Transcripts to Promote Breast Cancer Brain Metastasis

| PRJNA534211 | ENA

YTHDF3 Induces the Translation of m6A-enriched Metastasis-associated Gene Transcripts to Promote Breast Cancer Brain Metastasis [RIP-Seq]

Project description:YTHDF3 Induces the Translation of m6A-enriched Metastasis-associated Gene Transcripts to Promote Breast Cancer Brain Metastasis [RIP-Seq]

| PRJNA534213 | ENA

YTHDF3 improves translation initiation of mRNAs with N6-methyladenosine methylation at 5’ untranslated region by facilitating eIF2AK2 recruitment in oxaliplatin-resistant colorectal cancer - RIP-seq dataset

Project description:Oxaliplatin as a first-line drug frequently causes the chemo-resistance on colorectal cancer (CRC). N6-methyladenosine (m6A) methylation has been largely acknowledged in multiple biological functions. However, the molecular mechanisms underlying the m6A methylation in modulating anticancer drug resistance in CRC are still obscure. In present study, RIP-seq was conducted to investigate the occupancy of N6-methyladenosine RNA binding protein 3 (YTHDF3) served as “readers” that can recognize m6A modification site in HCT116 cells with oxaliplatin resistance (HCT116R). Then, YTHDF3 was knockdown by siRNA in HCT116 cells with oxaliplatin resistance, and RIP-seq was further conducted to investigate m6A methylation of HCT116, HCT116R and HCT116R cells with YTHDF3 knockdown.

2022-02-04 | E-MTAB-11321 | biostudies-arrayexpress

YTHDF3 facilitates translation and decay of the N6-methyladenosine-modified RNA

Project description:N6-methyladenosine (m6A) is the most abundant internal modification in eukaryotic messenger RNAs (mRNAs), and plays important roles in cell differentiation and organism development. It regulates multiple steps throughout the RNA life cycle including RNA processing, translation, and metabolism, via the recognition by selective binding proteins. In cytoplasm, m6A binding protein YTHDF1 facilitates translation of m6A-modified mRNAs, and YTHDF2 accelerates the decay of m6A-modified transcripts. The biological function of YTHDF3, another cytoplasmic m6A binder of the YTH domain family, remains unknown. Here, we report that YTHDF3 promotes protein synthesis in synergy with YTHDF1, and affects methylated mRNA decay mediated by YTHDF2. Cells deficient in all of YTHDF proteins experience the most dramatic accumulation of the m6A-methylated transcripts. These results indicate that in cytoplasm, YTHDF proteins act in an integrated and cooperative network to accelerate metabolism of m6A-modified mRNAs. The combinative and dynamic nature of YTHDF proteins may collectively impact fundamental biological processes and diseases related to m6A RNA methylation.

2016-09-15 | GSE86214 | GEO

m6A and YTHDF1, YTHDF2, YTHDF3 mapping of IAV RNA with PAR-CLIP and pA-m6A-seq

Project description:m6A and YTHDF1, YTHDF2, YTHDF3 mapping of IAV RNA with PAR-CLIP and pA-m6A-seq

2017-10-17 | GSE98033 | GEO

N6-Methyladenosine Reader YTHDF3-Mediated CEBPA Translation Maintains Genomic Stability and Stem Cells Function to Prevent Liver Injury and Hepatocellular Carcinoma [m6a-seq]

Project description:BACKGROUND & AIMS: Hepatocellular carcinoma (HCC) induced by chronic liver damage is a major cause of cancer mortality, but its precise epigenetic mechanisms are severely under studied. In addition, the role of N6-methyladenine (m6A) reader YTHDF3 in human diseases remains poorly understood. METHODS: Liver injury and hepatocarcinogenesis in mice were induced by chemical. CRISPR/Cas9 technology was used to construct Ythdf3 and Mettl14 knockout mice. Hepatic cell population characteristics was determined by means of 10X single-cell RNA-seq and flow cytometry. Cell proliferation and DNA damage were evaluated by immunofluorescence, immunohistochemistry, and western blot. Liver organoids were cultured to examine liver stem cells function. MeRIP-seq was used to reveal alterations in m6A methylation patterns impacted by chemical-induced liver injury. RIP-seq and Ribo-seq were applied to identify YTHDF3 targets and determine translation efficiency. Small interfering RNAs and dCas13b-FTO-sgRNA plasmids were used to evaluate the function of YTHDF3 and CEBPA in vitro. RESULTS: YTHDF3 depletion exacerbated chemical-induced liver injury with a reduction in functional hepatocytes and stem cells. Furthermore, METTL14 and YTHDF3-dependent RNA m6A dysregulation induced DNA damage and promoted development of HCC. Mechanistically, knockout of Ythdf3 impeded the translation of CCAAT/enhancer-binding protein-alpha (CEBPA), subsequently inhibited expression of PARP1 and PRDX2 to promote DNA damage and induce genomic instability, finally leading to liver injury and HCC. CONCLUSIONS: m6A/YTHDF3/CEBPA regulatory axis plays an essential role in governing cell fates and genomic stability, thereby preventing liver injury and HCC, and offers potential therapeutic avenue for targeting YTHDF3 and CEBPA in the treatment of HCC.

2024-02-29 | GSE259224 | GEO

YTHDF3 Induces the Translation of m6A-enriched Metastasis-associated Gene Transcripts to Promote Breast Cancer Brain Metastasis

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-09-30 | GSE130173 | GEO

YTHDF3 Induces the Translation of m<sup>6</sup>A-Enriched Gene Transcripts to Promote Breast Cancer Brain Metastasis.

Project description:Brain metastasis is a major cause of cancer mortality, but its molecular mechanisms are severely understudied. In addition, little is known regarding the role of m6A reader YTHDF3 in human diseases. Here, we show that YTHDF3 overexpression clinically correlates with brain metastases in breast cancer patients. YTHDF3 promotes cancer cell interactions with brain endothelial cells and astrocytes, blood-brain barrier extravasation, angiogenesis, and outgrow. Mechanistically, YTHDF3 enhances the translation of m6A-enriched transcripts for ST6GALNAC5, GJA1, and EGFR, all associated with brain metastasis. Furthermore, overexpression of YTHDF3 in brain metastases is attributed to increased gene copy number and the autoregulation of YTHDF3 cap-independent translation by binding to m6A residues within its own 5' UTR. Our work uncovers an essential role of YTHDF3 in controlling the interaction between cancer cells and brain microenvironment, thereby inducing brain metastatic competence.

| S-EPMC7738369 | biostudies-literature

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