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Role of FTO in ovarian cancer

ABSTRACT: Role of FTO in ovarian cancer

PROVIDER: PRJNA538933 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8959640.fastq.gz	Fastqsanger.gz
	SRR8959631.fastq.gz	Fastqsanger.gz
	SRR8959641.fastq.gz	Fastqsanger.gz
	SRR8959632.fastq.gz	Fastqsanger.gz
	SRR8959642.fastq.gz	Fastqsanger.gz

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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

Role of FTO in ovarian cancer (RNA-Seq)

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

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Role of FTO in ovarian cancer (MeRIP-Seq)

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

| PRJNA538931 | ENA

Role of FTO in ovarian cancer (RNA-Seq)

2020-07-01 | GSE130350 | GEO

Quantitative Proteomics of Mouse Liver (FTO-KO,WT) in response to DEN injection

Project description:Single nucleotide polymorphisms in the FTO gene encoding a m6A demthylase are associated with obesity and cancer development. However, the functional role of FTO in the developemnt of progression of hepatocellular carcinoma (HCC) as a proteotypic obesity-associated cancer remains unclear. Here, we have generated mice with hepatic FTO deficiency (FTOL-KO) and subjected them to DEN induced HCC-development. FTOL-KO mice exhibit increased HCC burden. While control mice exhibit a dynamic regulation of FTO upon induction of liver damage, this response is abrogated in mice lacking FTO. Proteomic analyses revealed that liver damage-induced increases in FTO expression promotes m6A-demethylation of CUL4A reducing its protein expression. Functionally, knockdown of CUL4A restores the increased hepatocyte proliferation observed upon loss of FTO. Collectively, our study reveals a protective role for FTO-dependent dynamic m6A mRNA demethylation of CUL4A in the initiation of HCC development.

2020-11-03 | PXD018223 | Pride

Knock down of FTO in cervical cancer cells

Project description:FTO, an N6-methyladenosine (m6A) demethylase, can promote cervical cancer cell proliferation and migration. RNA-sequencing of SiHa cells with FTO knockdown was conducted to dissect the differentially expressed genes and the potential mechanism of FTO in cervical cancer.

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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.

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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.

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Project description:Only a few studies have attempted to explore the potential role of FTO in gastric cancer, with one focusing on mitochondrial metabolism, while others have focused on the association of FTO with cell proliferation, migration, and invasion. To date, no study has comprehensively linked FTO-dependent m6A methylation to any form of cell death. We comprehensively explore the role of FTO-mediated m6A modification in gastric cancer ferroptosis by MeRIP-seq.

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