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Gene expression analysis of prostate cancer cells treated with fatty acid synthase (FASN) inhibitor IPI-9119

ABSTRACT: Gene expression analysis of prostate cancer cells treated with fatty acid synthase (FASN) inhibitor IPI-9119

PROVIDER: PRJNA454882 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7108420_1.fastq.gz	Fastqsanger.gz
	SRR7108420_2.fastq.gz	Fastqsanger.gz
	SRR7108430_1.fastq.gz	Fastqsanger.gz
	SRR7108430_2.fastq.gz	Fastqsanger.gz
	SRR7108440.fastq.gz	Fastqsanger.gz

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Gene expression analysis of prostate cancer cells treated with fatty acid synthase (FASN) inhibitor IPI-9119

Project description:Alterations in gene expression following fatty acid synthase inhibtion were evaluated in androgen sensitive LNCaP cells and castration resistant 22Rv1 and LNCaP-95 cells. Cell were exposed to 2 concentrations (0.1 and 0.5 uM) of FASN inhibitor IPI-9119 or DMSO for 6 days.

2019-01-17 | GSE114016 | GEO

FASN inhibition in prostate cancer cells C4-2

Project description:Fatty acid synthase (FASN) inhibition effect with IPI-9119 compound in prostate cancer cells C4-2

2024-02-01 | GSE224323 | GEO

Microarray gene expression profiling of transgenic mice with myocardium-specific over-expression of fatty acid synthase (FASN)

Project description:The fatty acid synthase (FASN) is the major fat synthesizing enzyme. FASN is an indispensable enzyme because mice with genetic deletion of Fasn are not viable. Apart from its physiological function, previous studies indicated that FASN could also exert a pathophysiological role, in the heart, because patients with heart failure showed up-reguation of FASN. To investigate the in vivo function of FASN up-regulation in the heart, we generated mice with myocardium-specific expression of FASN under control of the alpha-MHC promoter. Two different founder lines were generated with high and low FASN over-expression. Microarray gene expression profiling of heart tissue was performed of heart tissue from transgenic mice with high and low FASN expression Microarray gene expression profiling was performed with heart tissue isolated from three study groups: (i) Transgenic mice with high cardiac FASN expression, (ii) transgenic mice with low cardiac FASN expression, and (iii) B6 control mice.

2013-07-31 | E-GEOD-49351 | biostudies-arrayexpress

Genome-wide analysis of fatty acid synthase (FASN) gene silenced normal liver cells (THLE 2) using cDNA microarray analysis

Project description:Fatty acid synthase is a major enzyme involved in de novo lipogenesis, associated with energy homeostasis, lipid storage and signalling in normal liver cells. The effect of fatty acid synthase knockdown in normal liver cells (THLE 2) using siRNA mediated gene silencing were assesed for global gene deregulations. The deregulated metabolism, cell signalling and cell cycle pathway related gene expressions were analysed. Statistical significance values were also recorded. This expermental analysis clearly points to a important biochemical role for FASN in normal liver cell physiology. Total RNA was extracted from the THLE 2 cells transfected with FASN siRNA at 48h, along with its untransfected control cells. cDNA converted samples were run on microarray platform- Illumina HumanHT-12 V4.0 expression beadchip

2016-06-02 | E-GEOD-82096 | biostudies-arrayexpress

Microarray gene expression profiling of transgenic mice with myocardium-specific over-expression of fatty acid synthase (FASN)

2013-07-31 | GSE49351 | GEO

Genome-wide analysis of fatty acid synthase (FASN) gene silenced normal liver cells (THLE 2) using cDNA microarray analysis

2016-06-02 | GSE82096 | GEO

Role of fatty acid synthase in oligodendrocyte myelination

Project description:In the central nervous system, oligodendrocytes encase axons with myelin, a highly organized multilayered membrane structure. Myelin allows the rapid propagation of action potentials along the axons, while also supporting their mantainance metabolically. Fatty acids are basic building blocks for both glyco- and phospholipids, key constituents of cell membranes. Moreover, fatty acids can modify proteins via palmitoylation and activate transcriptional networks, e.g. through the PPARs transcription factors. Due to the high demand of membrane oligodendrocytes face to produce myelin, we hypothesized that they strongly rely upon fatty acid synthesis rather than mostly on their intake from the dietary pool. We tested this hypothesis by deleting the enzyme Fatty Acid Synthase specifically from neonatal oligodendrocyte progenitor cells, in vivo in C57Bl/6 olig2Cre FASN floxed mice. We addressed the consequences of this depletion on oligodendrocytes differentation and myelination potential in the central nervous system. In particular, we analyzed by RNA-seq how lack of FASN affected the transcriptome of optic nerves dissected from P14 mutant (olig2Cre FASN lox/lox) versus control (FASN lox/lox) mice.

2019-05-03 | GSE112725 | GEO

Fatty Acid Synthase Reprograms the Epigenome in Uterine Leiomyosarcomas

Project description:SK-UT-1 uterine leiomyosarcomas (Ut-LMS) cells were transduced with a fatty acid synthase (FASN)-containing retroviral vector to recapitulate the “lipogenic phenotype of cancer.” Consistent with this model, forced expression of FASN enhanced SK-UT-1 proliferation, migration, and cellular motion. Further investigation showed FASN promotes trimethylation of H3K9 (H3K9me3) and acetylation of H3K27 (H3K27ac) in SK-UT-1 cells. In contrast, siRNA targeting of FASN in high endogenous FASN expressing SK-LMS-1 Ut-LMS cells inhibits trimethylation of H3K9 and acetylation of H3K27. Palmitate, the predominant fatty acid product of FASN, increased H3K9me3, H3K27ac and H3K27me3 detection in SK-UT-1 cells. FASN promoted histone 3 methylation and acetylation through alteration of histone 3-modifying enzymatic activities (HDAC, HDM, HMT and HAT).ChIP-seq in SK-UT-1-FASN cells with anti-H3K9me3 antibody identified regions of enriched binding compared to vector-only cells. One differentially-enriched gene, CRISP1, was investigated further by ChIP-PCR. The transcriptionally repressive function of H3K9me3 was confirmed in CRISP1. Our results provide mechanistic insight into the pathobiology of the “lipogenic phenotype of cancer.” Here, FASN reprograms the Ut-LMS epigenome through chromatin remodeling to promote the “malignant phenotype.”

2017-06-14 | GSE98557 | GEO

Cigarette smoke promote the tumor progression via FASN in bladder cancer and rewiring the fatty acid metabolism

Project description:Cigarette smoke has been demonstrated to stimulate the growth of existing bladder tumors by enhancing the survival and proliferation of cancer cells through the action of carcinogens present in smoke. Concurrently, Fatty Acid Synthase (FASN), a key enzyme in fatty acid synthesis crucial for lipid metabolism, exhibits dysregulation in various cancer types, often correlating with aggressive phenotypes. In this study, we reveal altered fatty acid metabolism and elevated FASN and fatty acid levels, specifically in current smokers with bladder cancer (BLCA). Notably, increased FASN levels under smoke exposure are attributed to epigenetic alterations affecting fatty acid metabolism. Cells exposed to cigarette smoke demonstrate a metabolic shift in utilizing glutamine as a carbon source and producing fatty acids. The genetic and pharmacological inhibition of FASN effectively reduces tumor growth in a CAM model exposed to smoke. FASN inhibitors like TVB 2640, currently in phase II clinical trialsclinical trials in various cancer types, may be effective for smokers with BLCA exhibiting high FASN levels. In general, FASN inhibition offers therapeutic promise for mitigating the impact of cigarette smoke on bladder cancer progression.

2024-11-22 | GSE282144 | GEO

A bioorthogonal chemical reporter for fatty acid synthase-dependent protein acylation

Project description:Mammalian fatty acid synthase (FASN) is a lipogenic enzyme that catalyzes the formation of the long chain saturated fatty acid palmitate from acetyl and malonyl CoA in the presence of NADPH. Mammalian cells acquire fatty acids through dietary sources or through FASN. Although most mammalian cells express FASN at low levels, it is upregulated in cancers and during replication of many viruses. The precise role of FASN in disease pathogenesis is poorly understood, and whether de novo fatty acid synthesis contributes to host or viral protein acylation has been traditionally difficult to study. We describe a cell permeable, click-chemistry compatible alkynyl-acetate analog (5-Hexynoic acid, or "Alk-4") that functions as a reporter of FASN-dependent protein acylation. Alk-4 metabolic labeling enabled biotin-based purification and identification of more than 200 FASN-dependent acylated cellular proteins. Alk-4 also labeled the palmitoylated host protein IFITM3 (Interferon inducible transmembrane protein-3), a restriction factor for Influenza, and the myristoylated HIV-1 MA (Matrix) protein. Thus, Alk-4 is a useful bioorthogonal tool to selectively probe FASN-mediated protein acylation in normal and diseased states.

2022-02-15 | PXD028244 | Pride

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