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Sequencing of mRNA with N6-methyladenosine (m6A) modification in AML cells upon DMSO or FTO inhibitor treatment

ABSTRACT: To identify the potential mRNA targets of FTO inhibitor, we conducted m6A-seq with mRNA samples enriched from AML cells upon DMSO and FB23-2 (FTO inhibitor) treatment

ORGANISM(S): Homo sapiens

PROVIDER: GSE103496 | GEO | 2019/04/29

REPOSITORIES: GEO

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FTO demethyltion of N6-methyladenosine depends on the RRACH motif [m6A-seq]

Project description:The fat mass and obesity-associated (FTO) protein is a well-characterized demethylase that removes N6-methyladenosine (m6A) from animal mRNAs. However, it is unclear yet how the demethylation operates in living cells. In this study, we applied genome-wide approaches to study how FTO finds its demethylation targets in human cells. We overexpressed FTO in human HeLa cells, demonstrating that FTO effectively removes m6A from the RRACH motif enriched in the 3’UTR regions and leaves m6A at other motifs unaffected. RRACH elements are clearly enriched at FTO binding sites; however, m6A has a lower tendency to be removed from the FTO-bound RRACH. Taken together with the experimental validaton results, we propose a model in which FTO effectivly recognizes m6A-containing RRACH motifs in RNAs, leading to a faster demethylation and dissociation kinetic than the association, and consequently undectable FTO-mRNA association. However, when FTO binds to the non-m6A RRACH motif, the binding has a lower dissociation kinetics, yielding the detectable FTO binding signals which would enable FTO to have roles in regulating other mRNA processing events.

2020-03-22 | GSE101954 | GEO

N6-methyladenosine (m6A) sequencing of messenger RNAs in acute myeloid leukemia (AML) cells with and without knockdown of FTO

Project description:To identify potential mRNA targets of FTO whose m6A levels are influenced in acute myeloid leukemia (AML) cells, we conducted m6A-seq for mRNA isolated from MA9.3ITD cells with and without knockdown of FTO

2016-12-20 | GSE84944 | GEO

N6-methyladenosine modification is essential for prostate cancer cells

Project description:N6-methyladenosine (m6A) modification of messenger RNAs (mRNAs) is a pivotal mechanism controlling mRNA fate in cells. RNA m6A modification is regulated by the functional balance between methyltransferases and demethylases. Here we demonstrated that FTO-IT1 enhancer RNA (eRNA), a long non-coding RNA (lncRNA) transcribed from the last intron of FTO gene is significantly upregulated in CRPC and aggressive tumors compared to primary tumors. FTO-IT1 knockout by CRISPR/Cas9 almost completely blocks growth and G1-S cell cycle transition of both androgen-sensitive and castration-resistant prostate cancer cells. Meanwhile, the mRNA m6A was dramatically increased in FTO-IT knockout PCa cells and we identified FTO-IT1 as a binding partner of FTO. From m6A-seq, we unexpectedly found hypermethylated m6A associated with upregulated levels of the mRNAs for p53 signaling pathway genes in 22Rv1 prostate cancer cells. Mechanistic study showed that FTO-IT1 recruits FTO to the P53 target mRNA to promote their m6A demethylation, which leads to their degradation.

2023-07-09 | GSE189465 | GEO

FTO demethyltion of N6-methyladenosine depends on the RRACH motif [CLIP-seq]

2020-03-22 | GSE101953 | GEO

Sequencing of messenger RNAs with N6-methyladenosine modifications in acute myeloid leukemia (AML) with and without forced expression of FTO

Project description:To identify potential mRNA targets of FTO whose m6A levels are affected by FTO in acute myeloid leukemia (AML) cells, we conducted m6A-seq for messenger RNAs isolated from AML cells with and without forced expression of FTO.

2016-12-20 | GSE76414 | GEO

Structural Insights into N6-methyladenosine (m6A) Modification in the Transcriptome.

Project description: Not available

| S-EPMC6112310 | biostudies-literature

FTO regulates adult neurogenesis through modulating the dynamics of N6-methyladenosine

Project description:Fat mass and obesity-associated gene (FTO) is a member of the Fe (II) and oxoglutarate-dependent AlkB oxygenase family, and has been linked to obesity and intellectual disability. However, the role of FTO in neurodevelopment and neurogenesis remains largely unknown. Here, we show that FTO is expressed in adult neural stem cells (aNSCs) and neurons, and displays dynamic expression during postnatal neurodevelopment. The loss of FTO leads to the decreased brain size and body weight. We found that FTO deficiency could reduce the proliferation and neuronal differentiation of aNSCs in vivo, which leads to the impaired learning and memory. Given the role of FTO as a demethylase of N6-methyladenosine (m6A), we further performed the genome-wide m6A profiling and observed the dynamic m6A modification during postnatal neurodevelopment. The loss of FTO could lead to the altered m6A modifications on the mRNAs of several key components of BDNF pathway. These results together suggest that FTO play important roles in neurogenesis and learning and memory.

2017-04-20 | GSE94098 | GEO

N6-methyladenosine (m6A) modification and its clinical relevance in cognitive dysfunctions.

Project description: Not available

| S-EPMC8436914 | biostudies-literature

Sequencing of mRNAs with N6-methyladenosine modifications in Diabetic Nephropathy (DN) with and without forced expression of FTO

Project description:To identify potential mRNA targets of FTO whose m6A levels are affected by FTO in Diabetic Nephropathy (DN), we conducted m6A-seq for messenger RNAs isolated from HMC cells with and without forced expression of FTO.

2023-07-12 | GSE154561 | GEO

FTO Regulates Activation of Rho GTPases Signaling as N6-methyladenosine RNA Demethylase and an Rhotekin Partner Protein

Project description:Reversible RNA modification of N6-methyladenosine (m6A) plays a critical role in post-transcriptional gene regulation1-13. Although the fat mass and obesity-associated protein (FTO) has been previously shown to function as an m6A demethylase in nuclear RNA1,14, its exact function in disease pathogenesis remains a mystery. Here, we demonstrate that FTO suppresses the activation of Rho GTPase signaling via both its demethylation activity and specific interaction with Rho effector, Rhotekin (RTKN)15. The knockdown of FTO activates RhoA and RhoC, induces stress fibres, and accelerates cell migration. Endogenous RTKN is highly expressed in certain cancer and cancer-derived cell lines16,17 with overexpression of RTKN leading to moderate activation of Rho18. We further found that overexpression of RTKN blocks nuclear import of FTO and traps FTO in the cytoplasm to mediate m6A demethylation of cytosolic mRNA, thereby changing gene expression by preventing m6A-dependent mRNA decay and translation. Our results illustrate how FTO represses Rho activation through m6A demethylation and direct interaction with RTKN, and shed new light on FTO-dependent post-transcriptional gene regulation in RTKN overexpressed cancers, which may provide a new direction for developing anti-cancer therapies.

2018-12-31 | GSE83540 | GEO

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