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Targeting FTO suppresses hepatocellular carcinoma by inhibiting ERBB3 and TUBB4A expression [MeRIP]

ABSTRACT: Targeting FTO suppresses hepatocellular carcinoma by inhibiting ERBB3 and TUBB4A expression [MeRIP]

PROVIDER: PRJNA1116226 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29175338_1.fastq.gz	Fastqsanger.gz
	SRR29175338_2.fastq.gz	Fastqsanger.gz
	SRR29175339_1.fastq.gz	Fastqsanger.gz
	SRR29175339_2.fastq.gz	Fastqsanger.gz
	SRR29175340_1.fastq.gz	Fastqsanger.gz

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Targeting FTO suppresses hepatocellular carcinoma by inhibiting ERBB3 and TUBB4A expression [MeRIP]

Project description:Fat mass and obesity-associated protein (FTO) is an N6-methyladenosine (m6A) demethylase and plays a critical oncogenic role in various cancers. Here we show that FTO is an effective target in hepatocellular carcinoma (HCC). FTO is highly expressed in clinical patients of HCC and presents as a poor prognostic factor. Genetic depletion of FTO dramatically attenuated HCC progression in vivo. Pharmacological inhibition of FTO by FB23/FB23-2 remarkably suppressed the proliferation and migration of HCC cell lines in vitro, as well as inhibiting the HCC tumorigenicity in xeno-transplanted mice. Mechanistically, FB23-2 suppressed the expression of Erb-b2 receptor tyrosine kinase 3 (ERBB3) and human tubulin beta class Iva (TUBB4A) by increasing the m6A level in these mRNA transcripts. The decreased ERBB3 resulted in inhibited Akt-mTOR signaling that subsequently impaired the proliferation and survival of HCC cells. Moreover, FB23-2 abolished the organization of the tubulin cytoskeleton, while enforced expression of TUBB4A rescued the migration of HCC cells. Collectively, our study demonstrated that FTO plays a critical role in HCC by maintaining the proliferation and migration of cells, and highlights the broad potential of FTO inhibitors for targeting HCC.

2025-01-03 | GSE268330 | GEO

Targeting FTO suppresses hepatocellular carcinoma by inhibiting ERBB3 and TUBB4A expression [RNA-seq]

2025-01-03 | GSE268326 | GEO

Targeting FTO suppresses hepatocellular carcinoma by inhibiting ERBB3 and TUBB4A expression [RNA-seq]

Project description:Targeting FTO suppresses hepatocellular carcinoma by inhibiting ERBB3 and TUBB4A expression [RNA-seq]

| PRJNA1116222 | ENA

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 suppresses DNA repair by inhibiting PARP1

Project description:Maintaining genomic integrity and faithful transmission of genetic information are essential for the survival and proliferation of cells and organisms. DNA damage, which threatens the integrity of the genome, is rapidly sensed and repaired by mechanisms collectively known as DNA damage response in cells. Using an unbiased quantitative proteomic approach, we revealed the interactome of an RNA demethylase FTO (fat mass and obesity-associated protein). We identified a direct interaction with the DNA damage sensor protein PARP1 (poly-ADP-ribose polymerase 1), which dissociates upon ultraviolet (UV) stimulation. FTO inhibits PARP1 catalytic activity and controls its clustering in the nucleolus. Loss of FTO enhances PARP1 enzymatic activity and the rate of PARP1 recruitment to DNA damage sites, thus accelerating DNA repair and, consequently, cell survival. Thus, our study establishes FTO as an endogenous negative regulator of PARP1 and the UV-induced DNA damage response, which has implications for the treatment options of various cancers.

2025-03-26 | PXD041638 | Pride

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

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

2024-03-01 | GSE257546 | GEO

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

Project description: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.

2024-11-09 | GSE280813 | GEO

Role of FTO in ovarian cancer (MeRIP-Seq)

Project description:Role of FTO in ovarian cancer (MeRIP-Seq)

| PRJNA538931 | ENA