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Effect of FTO-KD on m6A modification in GH3 cell line [MeRIP-seq]

ABSTRACT: Effect of FTO-KD on m6A modification in GH3 cell line [MeRIP-seq]

PROVIDER: PRJNA1121217 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29317243_1.fastq.gz	Fastqsanger.gz
	SRR29317243_2.fastq.gz	Fastqsanger.gz
	SRR29317244_1.fastq.gz	Fastqsanger.gz
	SRR29317244_2.fastq.gz	Fastqsanger.gz
	SRR29317245_1.fastq.gz	Fastqsanger.gz

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Effect of FTO-KD on m6A modification in GH3 cell line [MeRIP-seq]

Project description:Growth hormone-secreting pituitary adenomas account for approximately 10% of endocrine pituitary tumors and are pathologically classified into densely granulated adenomas (DGGH) and sparsely granulated adenomas (SGGH). m6A has been reported to play an important role in tumorigenesis and development, but its potential role in the pathogenesis of these two subtypes has not yet been thoroughly investigated. Consequently, we performed MeRIP-seq analysis of pituitary adenomas and the GH3 cell line. We observed that the expression of FTO was significantly increased in SGGH, leading to a reduction in m6A modification and a disruption of desmosome organization.

2024-09-25 | GSE269321 | GEO

FTO suppresses cardiac fibrosis after myocardial infarction via m6A-mediated epigenetic modification [MeRIP-seq]

Project description:Cardiac fibrosis is common in cardiovascular diseases. N6-methyladenosine (m6A) is one of the most common modifications in eukaryotic mRNAs. Previous research has suggested that m6A modification is vital in cardiovascular diseases. The underlying targets of FTO were selected through transcriptome sequencing (RNA-seq) combined with methylated RNA immunoprecipitation sequencing (MeRIP-seq). According to MeRIP-seq and RNA-seq, FTO inhibited collagen synthesis in CFs.

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Effect of FTO-KD or FTO-OE on gene expression in GH3 cell line

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FTO suppresses cardiac fibrosis after myocardial infarction via m6A-mediated epigenetic modification

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Effect of FTO-KD or FTO-OE on gene expression in GH3 cell line

Project description:Effect of FTO-KD or FTO-OE on gene expression in GH3 cell line

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FTO suppresses cardiac fibrosis after myocardial infarction via m6A-mediated epigenetic modification [MeRIP-seq]

Project description:FTO suppresses cardiac fibrosis after myocardial infarction via m6A-mediated epigenetic modification [MeRIP-seq]

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M6A Demethylase FTO-mediated downregulation of DACT1 mRNA stability promotes Wnt signaling to facilitate osteosarcoma progression [MeRIP-seq]

Project description:Despite advances in clinical diagnosis and treatment, the prognosis of patients with osteosarcoma (OS) remains poor, and the treatment efficacy has plateaued. Therefore, it is important to identify new therapeutic targets for OS. N6-methyladenosine (m6A) modification has been reported to participate in tumor malignancy. In this study, functional screening found that the m6A demethylase FTO could be a candidate therapeutic target for OS. Upregulated FTO in OS could predict a poorer prognosis. FTO promoted the growth and metastasis of OS in vitro and in vivo. Methylated RNA immunoprecipitation sequencing (MeRIP-seq) and RNA sequencing (RNA-seq) were performed to identify DACT1 as a potential target of FTO. In vitro assays demonstrated that FTO could reduce the mRNA stability of DACT1 via m6A demethylation, which decreased DACT1 expression and further activated the Wnt signaling pathway. The oncogenic effect of FTO on OS was dependent on DACT1. In addition, the m6A reader IGF2BP1 was validated to participate in the regulation of DACT1. Entacapone, a conventional drug for Parkinson's disease, was confirmed to suppress OS via m6A-mediated regulation through the FTO/DACT1 axis. Our findings demonstrate that FTO may be a novel therapeutic target and that entacapone has the preclinical value to be repurposed for OS.

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Sequencing results of FTO overexpressing in papillary thyroid cells [meRIP-seq]

Project description:We tried to analyze the effect of FTO on papillary thyroid carcinoma. We constructed a FTO overexpression stable cell line of papillary thyroid carcinoma cells. We performed meRIP-seq sequencing analysis of the FTO overexpression stable transfer cell line to try to assess which genes were changed at the m6A level in papillary thyroid cancer cells by overexpressing FTO.

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m6A Modification Regulates Planarian Regeneration [MeRIP-seq]

Project description:m6A Modification Regulates Planarian Regeneration [MeRIP-seq]

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The Obesity-associated Fto gene regulates activity of the dopaminergic midbrain circuitry [FTO KO]

Project description:Here we use MeRIP-Seq to analyze global adenosine methylation (m6A) in mRNAs in the midbrain and striatum of Fto-deficient mice. We find that Fto deficiency leads to increased methylation within a subset of mRNAs important for neuronal signaling, including many within the dopaminergic signaling pathway. Collectively, our results show that Fto regulates demethylation of specific mRNAs in vivo, and this activity relates to control of dopaminergic transmission. Profiling of m6A in midbrain and striatum from FTO knockout mice

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