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Licochalcone B alleviates Crohn’s Disease injury by targeting FTO [meRIP-seq]

ABSTRACT: To investigate the mechanism of demethylase FTO in Crohn's disease，We used m6A MeRIP-seq data from three normal colon samples and three TNBS-induced IBD colon samples of C57 mice for gene expression profiling.

ORGANISM(S): Mus musculus

PROVIDER: GSE280813 | GEO | 2024/11/09

REPOSITORIES: GEO

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Licochalcone B alleviates Crohn’s Disease injury by targeting FTO [meRIP-seq]

Project description:Licochalcone B alleviates Crohn’s Disease injury by targeting FTO [meRIP-seq]

| PRJNA1180591 | ENA

Role of FTO in ovarian cancer (MeRIP-Seq)

Project description:RNA methylation plays an important role fine tuning translation and subsequently regulating cellular responses and cell fate. The fat mass- and obesity-associated protein (FTO) was recognized as an m6A demethylase and described as an oncogenic factor in leukemia and brain tumors. FTO expression levels are suppressed in ovarian tumors and ovarian cancer stem cells (CSCs). FTO induce cyclic AMP activity through targeting PDE4B and PDE1C by down-regulation of m6A levels in the mRNA transcript. In all or findings point to a tumor suppressor function of FTO in high grade serous OC

2020-07-01 | GSE130349 | GEO

FTO alleviates psoriasis-like dermatitis through the regulation of FN1

Project description:FTO was found to inhibit keratinocyte inflammation and proliferation in both in vitro and in vivo settings, independent of m6A demethylase function. RNA-seq was used to identify fibronectin (FN1,FN) as a potential target for FTO. FTO does not rely on demethylase activity to decrease FN1 expression. The anti-inflammatory and anti-proliferative effects of FTO on psoriasis partly depend on FN1. FTO may regulate the skipping of EDA exon in FN1.

2024-05-31 | GSE253791 | GEO

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.

2022-05-06 | GSE199205 | GEO

RNA seq and MeRIP-seq of COV434 cells before and after FTO knockdown

Project description:Multifunctional N6-methyladenosine (m6A) has been revealed to be an important epigenetic component in various physiological and pathological processes, but its role in female ovarian aging remains unclear. Thus, we demonstrated m6A demethylase FTO downregulation and the ensuing increased m6A in granulosa cells (GCs) of human aged ovaries, while FTO-knockdown GCs showed faster aging-related phenotypes mediated. Using the m6A-RNA-sequence technique (m6A-seq), increased m6A was found in the FOS-mRNA-3'UTR, which is suggested to be an erasing target of FTO that slows the degradation of FOS-mRNA to upregulate FOS expression in GCs, eventually resulting in GC-mediated ovarian aging. FTO acts as a senescence-retarding protein via m6A, and FOS knockdown significantly alleviates the aging of FTO-knockdown GCs.

2021-06-15 | GSE178095 | GEO

Adiponectin-cre FTO flox/flox and FTO flox/flox mouse white fat tissues

Project description:Single nucleotide polymorphisms in intron 1 of the fat mass and obesity-associated (FTO) gene were found to be associated with an increased risk of adult obesity. Enhanced FTO expression in mice leads to hyperphagia, increased fat mass, and higher body weight. Neuronal-specific FTOâ??deleted mice have an identical lean body weight phenotype to global FTO-deleted mice. The physiological role of adipose FTO in the homeostasis of energy regulation remains to be elucidated. We used microarrays to elucidate the metabolic pathways that are regulated by FTO in the white fat. FTO flox/flox and Adiponectin-cre FTO flox/flox (AFO) mice were fed with chow diet. White fat tissues from epididymal adipose pad were harvested under ad lib condition for RNA isolation. Three independent pools of FTO flox/flox and AFO mouse white fat RNA were included in the study.

2016-07-03 | E-GEOD-65098 | biostudies-arrayexpress

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

2013-06-15 | E-GEOD-47216 | biostudies-arrayexpress

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.

2024-03-03 | GSE259328 | GEO

FTO-mediated autophagy inhibition promotes non-small cell lung cancer progression by reducing SESN2 mRNA stability [MeRIP-Seq]

Project description:N6-methyladenosine (m6A) serves as the most abundant mRNA modification within eukaryotes that is involved in autophagy and progression of non-small cell lung cancer (NSCLC). The role of the m6A demethylase FTO in NSCLC progression has recently received widespread attention. However, the mechanism of FTO-mediated autophagy regulation in NSCLC progression is unclear. In this study, we found that FTO was significantly up-regulated in NSCLC, and down-regulation of FTO blocked the growth, invasion and migration of NSCLC cells via autophagy induction. Importantly, SESN2 was involved in m6A regulation during autophagy in NSCLC cells. FTO deficiency prompted IGF2BP1 to interact with SESN2 mRNA, which led to an increase in SESN2 mRNA stability as well as enhanced SESN2 protein levels. However, FTO inhibited autophagic flux via down-regulation of SESN2, thereby promoting the growth, invasion and migration of NSCLC cells. Our findings uncovered that FTO-mediated autophagy inhibition promotes malignant progression of NSCLC via reduction of SESN2 mRNA stability, thus providing novel notions for the prevention and treatment of NSCLC.

2024-03-09 | GSE240879 | GEO

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.

2024-11-30 | GSE189877 | GEO

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