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Macrophage-derived cholesterol contributes to therapeutic resistance in prostate cancer

ABSTRACT: Macrophage-derived cholesterol contributes to therapeutic resistance in prostate cancer

PROVIDER: PRJNA747294 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15178341_1.fastq.gz	Fastqsanger.gz
	SRR15178341_2.fastq.gz	Fastqsanger.gz
	SRR15178342_1.fastq.gz	Fastqsanger.gz
	SRR15178342_2.fastq.gz	Fastqsanger.gz
	SRR15178343_1.fastq.gz	Fastqsanger.gz

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Macrophage-derived cholesterol contributes to therapeutic resistance in prostate cancer

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Project description:Understanding the systemic regulation of normal prostate gene expression by cholesterol diet is critical for deciphering the mechanisms responsible for the transition from healthy to pathogenic prostate conditions. To understand mechanism under cholesterol effect on prostate, we performed microarray analysis using prostate tissues from SCID or C57BL/6 mice feed with varying diet conditions containing high, low or normal cholesterol. The RNA is obtained from ventral prostate (VP), dorsal lateral prostate (DLP), and anterior prostate (AP) in 18 SCID mice.

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Project description:This SuperSeries is composed of the following subset Series: GSE25461: Gene expression of three prostate lobes, ventral prostate (VP), dorsal lateral prostate (DLP), and anterior prostate (AP), by cholesterol diet GSE25472: Gene expression of LNCaP human prostate cells by cholesterol diet Refer to individual Series

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DNA methyltransferase 1 deficiency improves macrophage motility and wound healing by ameliorating cholesterol accumulation

Project description:Healing of the cutaneous wound requires macrophage recruitment at the sites of injury, where chemotactic migration of macrophages toward the wound is regulated by local inflammation. Recent studies suggest a positive contribution of DNA methyltransferase 1 (Dnmt1) to macrophage pro-informatory responses; however, its role in regulating macrophage motility remains unknown. In this study, myeloid-specific depletion of Dnmt1 in mice promoted cutaneous wound healing and de-suppressed the lipopolysaccharides (LPS)-inhibited macrophage motility. Dnmt1 inhibition in macrophages eliminated the LPS-stimulated changes in cellular mechanical properties in terms of elasticity and viscoelasticity. LPS increased the cellular accumulation of cholesterol in a Dnmt1-depedent manner; cholesterol content determined cellular stiffness and motility. Lipidomic analysis indicated that Dnmt1 inhibition altered the cellular lipid homeostasis, probably through down-regulating the expression of cluster of differentiation 36 CD36 (facilitating lipid influx) and up-regulating the expression of ATP-binding cassette transporter ABCA1 (mediating lipid efflux) and sterol O-acyltransferase 1 SOAT1 (also named ACAT1, catalyzing the esterification of cholesterol). Our study revealed a Dnmt1-dependent epigenetic mechanism in the control of macrophage mechanical properties and the related chemotactic motility, indicating Dnmt1 as both a marker of diseases and a potential target of therapeutic intervention for wound healing.

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Transcriptional regulation of macrophage cholesterol efflux and atherogenesis by a long noncoding RNA

Project description:Nuclear receptors are important conduits between environmental cues and gene expression, but the molecular events governing spatial variation in their responses remain poorly understood. Here we outline an important role for a non-coding RNA in modulating the cell type-specific actions of the cholesterol-activated nuclear receptor LXR. LXR regulates the expression of genes involved in responses to excess cholesterol and has been causally linked to the pathogenesis and treatment of prevention and atherosclerosis in animals. We identify the lncRNA MeXis as an amplifier of LXRdependent transcription of the critical cholesterol efflux gene Abca1. MeXis interacts with and guides the promoter binding of the nuclear receptor transcriptional coactivator DDX17. Loss of MeXis in murine immune cells has a marked impact on chromosome architecture at the Abca1 locus, impairs cellular responses to cholesterol overload, and accelerates the development of atherosclerosis. Our findings define MeXis as a lncRNA gatekeeper that modifies the actions of LXR in lipid-dependent control of macrophage gene expression. This has important implications for mechanisms that underlie spatial activation patterns of nuclear receptors. Our work opens a new gateway to targeting reverse cholesterol transport since it is conceivable that therapeutic approaches that enhance MeXis activity might reduce foam cell formation and atherogenesis

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