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Effective FTO inhibitors with potent anti-tumor efficacy suppress cancer stem/initiating cell self-renewal and overcome immune evasion

ABSTRACT: Effective FTO inhibitors with potent anti-tumor efficacy suppress cancer stem/initiating cell self-renewal and overcome immune evasion

PROVIDER: PRJNA561592 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10044645.fastq.gz	Fastqsanger.gz
	SRR10044646.fastq.gz	Fastqsanger.gz
	SRR10044647.fastq.gz	Fastqsanger.gz
	SRR10044648.fastq.gz	Fastqsanger.gz
	SRR10044649.fastq.gz	Fastqsanger.gz

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Similar Datasets

Effective FTO inhibitors with potent anti-tumor efficacy suppress cancer stem/initiating cell self-renewal and overcome immune evasion

Project description:We conducted RNA sequencing with poly A RNA isolated from NOMO-1 cells upon shRNA induced FTO knockdown and small molecules (CS1 and CS2) mediated FTO inhibition .

2020-04-11 | GSE136204 | GEO

Targeting FTO suppresses cancer stem cell maintance and immune evasion

Project description:Targeting FTO suppresses cancer stem cell maintance and immune evasion

| PRJNA606960 | ENA

Tumors exploit FTO-mediated regulation of glycolytic metabolism to evade immune surveillance

Project description:Ever-increasing understanding about the complexity of factors and regulatory layers that contribute to immune evasion facilitates the development of immunotherapies. However, the diversity of malignant tumors limits many known mechanisms in specific genetic and epigenetic contexts, manifesting the need to discover general driver genes. Here, we have identified the m6A demethylase FTO as an essential epitranscriptomic regulator utilized by tumors to escape immune surveillance through regulation of glycolytic metabolism. We show that FTO-mediated m6A demethylation in tumor cells elevates transcription factors c-Jun, JunB, and C/EBPβ, which allows the rewiring of glycolytic metabolism. Fto knockdown impairs the glycolytic activity of tumor cells, which restores the function of CD8+ T cells, thereby inhibiting tumor growth. Furthermore, we developed a small-molecule compound Dac51 that can inhibit the activity of FTO, block FTO-mediated immune evasion, and synergize with checkpoint blockade for better tumor control, suggesting reprogramming RNA epitranscriptome as a potential strategy for immunotherapy.

2021-04-30 | GSE154952 | 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

Targeting FTO suppresses cancer stem cell maintance and immune evasion

Project description:We conducted RNA sequencing with poly A RNA isolated from spleen mononuclear cells of MLL-AF9 (MA9) mouse models after treatment with PBS and FTO inhibitor CS1.

2020-04-11 | GSE145363 | 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 over expression in mice

Project description:In this study, we aimed to examine the changes in gene expression that occur in FTO over expressing mice in order to gain more insight into the underlying mechanisms by which FTO influences body weight and adiposity

2014-06-01 | E-MTAB-2331 | biostudies-arrayexpress

Effect of FTO overexpression and knockdown on transcriptome of HEK293 cells

Project description:To gain insight into FTO function, we knocked down and overexpressed FTO in HEK293 cells.Genetrail analyses of expression profiles pointed to the RNA splicing and processing machinery. Intriguingly, using immunocytochemistry and confocal laser scanning microscopy, we observed strong enrichment of FTO in nuclear speckles and - to a lesser extent - in nucleoli, but not in other known nuclear bodies. We also studied RNA samples of Fto knockout and wild type mice with regard to content of methylated and unmethylated nucleosidesand observed that ratios of modified and unmodified uracil and adenine were different depending on the presence of FTO. Taken together, our data suggest that FTO is involved in RNA processing and modification. We used microarrays to investigate global gene expression changes depending on the level of FTO We compared FTO overexpressing and FTO depleted cells to cells with endogeneus level of FTO to determine global gene expression changes.

2012-11-13 | E-GEOD-33870 | biostudies-arrayexpress

FTO: gene expression and function in skeletal muscle

Project description:We identified the target genes of FTO ("fat mass and obesity associated") in primary cultures of human skeletal muscle cells using adenoviral vectors expressing FTO or GFP and oligonucleotide microarrays. Human myotubes were prepared from 4 different skeletal muscle biopsies. After differentiation, myotubes were infected for 48 hours with recombinant adenovirus expressing either GFP or FTO. Each FTO-infected myotubes culture was compared to GFP-infected myotubes culture. GFP-infected myotubes were regarded as the control. Four biological replicates were processed.

2011-07-05 | E-GEOD-22857 | biostudies-arrayexpress

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

2016-01-01 | GSE65098 | GEO