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Palmitic acid regulates the biological function of Ovarian Cancer

ABSTRACT: Palmitic acid regulates the biological function of Ovarian Cancer

PROVIDER: PRJNA1170854 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30920706_1.fastq.gz	Fastqsanger.gz
	SRR30920706_2.fastq.gz	Fastqsanger.gz
	SRR30920707_1.fastq.gz	Fastqsanger.gz
	SRR30920707_2.fastq.gz	Fastqsanger.gz
	SRR30920708_1.fastq.gz	Fastqsanger.gz

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Palmitic acid regulates the biological function of Ovarian Cancer

Project description:Palmitic acid was positively correlated with the invasion ability of ovarian cancer cells, its up-regulation inhibited the migrative, invasive and cloning capacity of cancer cells in vitro and suppressed the tumor proliferation and intraperitoneal diffusion in vivo, while its up-regulation did the opposite.

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Effect of Palmitic acid on the transcriptional profile of skin regulatory T cells (Tregs)

Project description:We found that palmitic acid inhibits proliferation and cell death of Tregs in the skin. The goal of this study is to investigate how Palmitic acid drives lipid toxicity in skin Tregs

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Effect of palmitic acid on gene expression of two types of endothelial cells

Project description:To investigate the effect of palmitic acid on gene expression of rat corpus cavernosum endothelial cells (RCCECs) and human umbilical vein endothelial cells (HUVECs), we used palmitic acid to treat these two primary cells, which were then subjected to RNA-seq.

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Effect of exogenous FABP4 (A-FABP/aP2) with and without palmitic acid on gene expression in RAW264.7 macrophages

Project description:Gene expression profile of FABP4 treatment in RAW264.7 macrophages was examined to show a ligand (palmitic acid)-dependent and a ligand-independent effect of FABP4. RAW264.7 macrophages were treated with and without 200 nM recombinant FABP4 in the absence and presence of 0.2 mM palmitic acid.

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Palmitic Acid Upregulates Type I Interferon-Mediated Antiviral Response and Cholesterol Biosynthesis in Human Astrocytes

Project description:Chronic intake of a high-fat diet increases saturated fatty acids in the brain causing the progression of neurodegenerative diseases. Palmitic acid is a free fatty acid abundant in the diet that at high concentrations may penetrate the blood brain barrier and stimulate the production of pro-inflammatory cytokines, leading to inflammation in astrocytes. The use of the synthetic neurosteroid tibolone in protection against fatty acid toxicity is emerging, but its transcriptional effects on palmitic acid induced lipotoxicity remain unclear. Herein, we performed a transcriptome profiling of normal human astrocytes to investigate the molecular mechanisms by which palmitic acid causes cellular damage to astrocytes, and whether tibolone could reverse its detrimental effects. Astrocytes undergo a profound transcriptional change at 2 mM palmitic acid, affecting the expression of 739 genes, 366 upregulated and 373 downregulated. However, tibolone at 10 nM does not entirely reverse palmitic acid effects. Additionally, the protein protein interaction reveals two novel gene clustering modules. The first module involves astrocyte defense responses by upregulation of pathways associated with antiviral innate immunity, and the second is linked to lipid metabolism. Our data suggest that activation of viral response signaling pathways might be so far, the initial molecular mechanism of astrocytes in response to a lipotoxic insult by palmitic acid, triggered particularly upon increased expression levels of *IFIT2*, *IRF1*, and *XAF1*. Therefore, this novel approach using a global gene expression analysis may shed light on the pleiotropic effects of palmitic acid on astrocytes, and provide a basis for future studies addressed to elucidate these responses in neurodegenerative conditions, which is highly valuable for the design of therapeutic strategies.

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