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Role of FTO in ovarian cancer (MeRIP-Seq)

ABSTRACT: 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

ORGANISM(S): Homo sapiens

PROVIDER: GSE130349 | GEO | 2020/07/01

REPOSITORIES: GEO

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Role of FTO in ovarian cancer (RNA-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. 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 | GSE130350 | 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

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

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 interacted proteins of ALKBH5 and FTO identified by IP-mass

Project description:Since m6A demethylases (FTO and ALKBH5) have been reported to be involved in pre-mRNA splicing regulation, we hypothesized that dynamic m6A distribution during mRNA maturation might involve removal of m6A in internal exons by FTO or ALKBH5 accompanied by splicing factors. To explore this we performed pull-down assays coupled with protein mass spectrometry.

2022-12-09 | PXD038705 | Pride

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

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

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

2013-06-15 | E-GEOD-47215 | biostudies-arrayexpress

m6A alterations through FTO in breast cancer [RNA-seq]

Project description:Our understanding of posttranscriptional modifications that decorate RNA, a regulatory layer positioned between DNA and proteins, is in its infancy. N6-methyladenosine (m6A) is the most prevalent internal modification in messenger RNAs that is installed and erased by m6A methyltransferases and demethylases. The importance of these enzymes in cancer is rapidly emerging, yet information of their specific mode of actions during disease progression remain largely unknown. In the present study, we report that the m6A RNA demethylase FTO controls EMT and invasion in cancer through regulation of the Wnt pathway. We find that loss of FTO, in contrast to acute myeloid leukemia, is frequent in many cancer types, including breast and prostate cancers. Knockdown of FTO promotes tumor progression – specifically migration and invasion – in breast and prostate cancer cells. Furthermore, implantation of these cells accelerates tumor progression in recipient mice in vivo. In these tumors, FTO depletion leads to m6A-dependent activation of Wnt signaling, which drives an enhanced EMT program and invasion, thus leading to poor clinical outcome. However, loss of FTO also sensitizes cancers cells to Wnt inhibition, offering a rationale for the therapeutic targeting of Wnt for cancer patients with low FTO levels. Together, our work reveals FTO as a novel regulator of EMT and an unexpected mechanism by which Wnt signals are dysregulated in tumors, providing a rationale to stratify cancer patients treated with Wnt inhibitor. These data uncover a previously unrecognized relationship between RNA modification and EMT in cancer.

2021-01-11 | GSE128581 | GEO

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