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Tumor-induced cholesterol efflux from macrophages drives IL-4 mediated reprogramming and tumor progression

ABSTRACT: Tumor-induced cholesterol efflux from macrophages drives IL-4 mediated reprogramming and tumor progression

PROVIDER: PRJNA521733 | ENA |

REPOSITORIES: ENA

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Tumor-induced cholesterol efflux from macrophages drives IL-4 mediated reprogramming and tumor progression

Project description:Tumor-associated macrophages (TAM) have been shown to have important roles in the malignant progression of various cancers. However, macrophages also posses intrinsic tumoricidal activity and can promote the activity of cytotoxic lymphocytes, but they rapidly adopt an alternative phenotype within tumors, associated with immune-suppression and trophic functions that support tumor growth. The mechanisms that promote TAM polarization in the tumor-microenvironment remain poorly understood, these mechanisms may represent important therapeutic targets to block the tumor-promoting functions of TAM and restore their anti-tumor potential. Here we have characterized TAM in a mouse model of metastatic ovarian cancer. We show that ovarian cancer cells promote membrane-cholesterol efflux and the depletion of lipid rafts from macrophages. Increased cholesterol efflux promoted IL-4 mediated reprogramming while inhibiting IFNg-induced gene expression. These studies reveal an unexpected role for tumor-induced membrane-cholesterol efflux in driving the IL-4 signaling and the tumor-promoting functions of TAM, while rendering them refractory to pro-inflammatory stimuli. Thus, preventing cholesterol efflux in TAM could represent a novel therapeutic strategy to block pro-tumor functions and restore anti-tumor immunity.

2019-11-28 | GSE126378 | GEO

Gene expression profile at single cell level of lung-tumor bearing KrasG12D mice with or without defective cholesterol efflux

Project description:Impaired cholesterol efflux pathways is a hallmark of lung adenocarcinoma. We used single cell RNA sequencing (scRNA-seq) to analyze the impact of defective cholesterol efflux on cell diversity in lung tumor

2023-06-01 | GSE226597 | GEO

Hepatic steatosis promotes atherosclerosis progression via extracellular vesicles mediated inhibition of cholesterol efflux in foam cells

Project description:To determine the functional miRNA mediated the inhibition role of exosomes (EVs) on the, cholesterol efflux, miRNA sequencing was conducted to compare the expression profile of miRNA content in EVs isolated from primary hepatocytes of chow diet-fed ApoE-/- mice (Chow-EVs) or HFHC-fed ApoE-/- mice (HFHC-EVs).

2023-10-18 | GSE232919 | GEO

LXR Suppresses Inflammatory Gene Expression and Neutrophil Migration through cis-Repression and Cholesterol Efflux [ATAC-Seq]

Project description:The activation of Liver X Receptor (LXR) promotes cholesterol efflux and repression of inflammatory genes with anti-atherogenic consequences. The mechanisms underlying repressive activity of LXR are controversial and have been attributed to cholesterol efflux or to transrepression of Activator Protein-1 (AP-1) activity. Here, we find that cholesterol efflux contributes to LXR repression, while direct repressive functions of LXR also play a key role but are independent of AP-1. We use ATAC-seq to show that LXR reduces chromatin accessibility in cis at inflammatory gene enhancers containing LXR binding sites. Targets of this repressive activity are associated with leukocyte adhesion and neutrophil migration, and LXR agonist treatment suppresses neutrophil recruitment in a mouse model of sterile peritonitis. These studies suggest a model of repression in which liganded LXR binds in cis to canonical nuclear receptor binding sites and represses pro-atherogenic leukocyte functions in tandem with induction of LXR targets mediating cholesterol efflux.

2018-11-17 | GSE109998 | GEO

LXR Suppresses Inflammatory Gene Expression and Neutrophil Migration through cis-Repression and Cholesterol Efflux [RNA-Seq]

2018-11-17 | GSE109997 | GEO

Apolipoprotein A1-Manipulated Cholesterol Efflux Subverts the Phagocytic Fragility of TAMs and Improves Oncolytic Viro-Immunotherapy in Glioblastoma [Tumor RNA-seq]

Project description:We found that overexpression of APOA1 in glioblastoma (GBM) promotes cholesterol efflux from TAMs and restores phagocytosis and antigen presentation. Therefore, we constructed a recombinant oncolytic adenovirus expressing APOA1 to carry the cholesterol regulatory elements of TAMs. AdV-APOA1 exhibited better antitumor effects than AdV-Ctrl in several orthotopic GBM tumor models. Further, we collected virus-treated GL261-CAR tumors for RNA-seq to reveal differences in biological processes between them. Specifically, intracranial 14-day GL261-CAR-bearing C57BL/6J mice were i.t. injected with 1 × 108 PFU AdV-Ctrl or 1 × 108 PFU AdV-APOA1. The tumor bulks were then collected to perform transcriptome RNA-seq analysis 3 days after virus injection.

2022-05-04 | GSE201976 | GEO

Apolipoprotein A1-Manipulated Cholesterol Efflux Subverts the Phagocytic Fragility of TAMs and Improves Oncolytic Viro-Immunotherapy in Glioblastoma [BMDMs RNA-seq]

Project description:We found that TAMs in the glioblatoma (GBM) tumor microenvironment are enriched for cholesterol and highly express ABCA1/G1. To investigate the biological effects of enhancing cholesterol efflux of TAMs in GBM, we constructed APOA1-overexpressing GL261 cell line. We harvested tumor tissue and sorted these TAMs by anti-mouse F4/80 magnetic beads 17 days after intracranial transplantation of GL261-APOA1 cell line and control cells in immunocompetent C57 mice. Samples were subjected to transcriptome sequencing.

2022-10-09 | GSE214907 | GEO

Apolipoprotein A1-Manipulated Cholesterol Efflux Subverts the Phagocytic Fragility of TAMs and Improves Oncolytic Viro-Immunotherapy in Glioblastoma [TAMs RNA-seq]

2022-05-04 | GSE201975 | GEO

Effects of deletioin of cholesterol efflux genes Abca1 and Abcg1 on other gene expressions in macrophages

Project description:ATP binding cassette subfamily member 1 (ABCA1) and G1 (ABCG1) are cholesterol efflux transporter to prevent excess intracellular cholesterol accumulation. We here report the deletion of Abca1 and Abcg1 results in the significant increased expression of Cd38, a multi-faceted ectoenzyme with NADase activity.

2024-04-17 | GSE234507 | GEO

Intracoronary imaging, cholesterol efflux and transcriptomes after intensive statin treatment

Project description:The relation of serial changes in plaque morphology of obstructive nonculprit lesions to HDL efflux, inflammation and transcriptome perturbations in response to high-dose statin therapy (YELLOW II study). YELLOW II is a prospective single center study. Stable patients who were scheduled for elective coronary angiography and/or coronary artery stenting were screened for this study. The final target population were patients with multivessel disease requiring staged intervention, culprit vessel initially and non-culprit vessel later, with maxLCBI4mm greater than 150 by NIRS. Patients underwent PCI for a culprit lesion followed by OCT and NIRS/IVUS of an obstructive non-culprit lesion (NCL). All subjects received rosuvastatin, 40 mg every day for 8-12 weeks. The NCL was reimaged and underwent intervention as a part of staged intervention. Blood samples were obtained for cholesterol efflux capacity (CEC) quantification and peripheral PBMC isolation. Despite the extensive evidence for the beneficial effects of statins on clinical outcomes, the mechanisms underlying these effects in remain elusive. In a prospective study, 85 patients with stable multivessel coronary artery disease underwent percutaneous coronary intervention for a culprit lesion followed by intracoronary multi-modality imaging including optical coherence tomography (OCT) of an obstructive NCL. All subjects received 40 mg of rosuvastatin every day for 8-12 weeks, when the NCL was reimaged and intervention was performed. Blood samples were drawn at both times to assess cholesterol efflux capacity (CEC) and transcriptomic profile in peripheral blood mononuclear cells (PBMC).

2016-10-29 | GSE86216 | GEO

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