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Enhancer RNA transcription defines novel CSF1 enhancer in triple-negative breast cancer

ABSTRACT: We report the results of employing CRISPR interference (CRISPRi) to epigenetically perturb the CSF1 transcription start site or novel CSF1 enhancer, followed by high-throughput RNA-sequencing to identify downstream gene expression changes in human triple negative breast cancer cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE185318 | GEO | 2022/04/12

REPOSITORIES: GEO

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Enhancer RNA transcription defines novel CSF1 enhancer in triple-negative breast cancer

Project description:Enhancer RNA transcription defines novel CSF1 enhancer in triple-negative breast cancer

| PRJNA768668 | ENA

RNAseq of untreated and CSF1-treated, CSF1+QVD-treated monocytes

Project description:Caspases, which are key effectors of apoptosis, have demonstrated non-apoptotic functions. One of these functions is the differentiation into macrophages of peripheral blood monocytes exposed to Colony-Stimulating Factor-1 (CSF1). Macrophage polarization plays an important role in the pathogenesis of diverse human diseases as cancer, leading us to explore if caspase inhibition would affect macrophage polarization. To explore the role of caspases in CSF1 differentiation, we used human monocytes sorted from buffy coats treated by cytokines. We reported that caspase inhibition delays the ex vivo differentiation of peripheral blood monocytes exposed to CSF1 and modifies the phenotype of generated macrophages, e.g. cell shape, surface markers. Moreover, by RNAseq, we observed that the macrophages generated in presence of CSF1 and QVD are different from CSF1-treated monocytes. This study confirms the importance of caspase activation in CSF1 differentiation.

2024-01-01 | E-MTAB-8088 | biostudies-arrayexpress

RNAseq of untreated, CSF1-treated, CSF1+QVD-treated, and GM-CSF-treated monocytes

Project description:Caspases, which are key effectors of apoptosis, have demonstrated non-apoptotic functions. One of these functions is the differentiation into macrophages of peripheral blood monocytes exposed to Colony-Stimulating Factor-1 (CSF1). Conversely, GM-CSF induces the differentiation of monocytes into macrophages in a caspase-independent manner. Macrophages generated by CSF1 and GM-CSF have distinct polarity. Macrophage polarization plays an important role in the pathogenesis of diverse human diseases as cancer, leading us to explore if caspase inhibition would affect macrophage polarization. To explore the role of caspases in CSF1 differentiation, we used human monocytes sorted from buffy coats treated by cytokines. We reported that caspase inhibition delays the ex vivo differentiation of peripheral blood monocytes exposed to CSF1 and modifies the phenotype of generated macrophages, e.g. cell shape, surface markers. Moreover, by RNAseq, we observed that the macrophages generated in presence of CSF1 and QVD are different from CSF1-treated monocytes and from GM-CSF-treated monocytes. Cell cycle and focal adhesion-related pathway genes were selectively down-regulated. This study confirms the importance of caspase activation in CSF1 differentiation.

2024-01-01 | E-MTAB-5752 | biostudies-arrayexpress

RNA-seq of CSMD1 enhancer CRISPRi in LUHMES cells and differentiated neurons

Project description:we performed lentiviral CRISPR interference (CRISPRi) by recruiting dCas9 fused with the KRAB domain to the CSMD1 enhancer (fam3) in the neuronal precursor cell line – Lund human mesencephalic (LUHMES). Given that the expression of CSMD1 was not detectable in LUHMES cells we differentiated these cells into neurons. Differentiated neurons with CRISPRi of CSMD1 enhancer showed significantly higher expression of CSMD1 than control.

2022-06-30 | E-MTAB-8027 | biostudies-arrayexpress

The effect of CSF1-Fc treatment in pigs on liver gene expression

Project description:The expression was designed to determine whether exposure to CSF1-Fc has any effect on liver-specific gene expression in pigs. livers from pigs exposed to CSF1-Fc

2016-08-01 | E-GEOD-78837 | biostudies-arrayexpress

Expression data from CSF1- or CSF2-induced bone marrow derived macrophages (BMDMs): M(CSF1) and M(CSF2) cells.

Project description:Femur and tibia bones were harvested from 8-week-old wild-type (WT) C57BL/6 mice. Bone marrow was flushed out into cold PBS (Life Technologies) plus 2% heat-inactivated FBS, passed through a needle five times to dissociate the cells, and then passed through a 70-μm cell strainer (Becton Dickinson) to remove cell clumps, bone, hair, and other cells/tissues. After addition of three volumes of NH4Cl solution (0.8% NH4Cl solution; Beyotime Institute of Biotechnology, Jiangsu, China), the mixture was incubated on ice for 10 min to remove red blood cells; the cells were then spun down and resuspended in cold PBS with 2% FBS. The harvested cells were cultured in DMEM containing 10% FBS and supplemented with 10 ng/ml recombinant mouse CSF1 (R&D Systems) or 10 ng/ml recombinant mouse CSF2 (R&D Systems) for 7 days to obtain CSF1- or CSF2-induced BMDMs: M(CSF1) or M(CSF2) cells, respectively. To test the difference genes expression of TAMs obtained from M(CSF1) and M(CSF2) cells in C57BL/6 mice. We used microarrays to detail the global programme of gene expression and identified M(CSF1) and M(CSF2) cells during this process.

2017-02-28 | GSE95404 | GEO

Microglial responses to CSF1 overexpression do not promote expansion of other glial lineages

Project description:CSF1 expression in the central nervous system (CNS) increases in response to a variety of stimuli, and CSF1 is overexpressed in many CNS diseases. In young adult mice we previously showed that CSF1 overexpression in the CNS caused proliferation of IBA1+ microglia without promoting expression of M2 polarization markers. Here we further examine the impacts of increased CSF1 levels in the brain. As CSF1 over-expressing mice age, IBA1+ cell numbers are constrained by a decline in proliferation rate. Compared to controls, there were no differences in expression of the M2 markers ARG1 and MRC1 (CD206) in CSF1 overexpressing mice of any age, indicating that even prolonged exposure to increased CSF1 is not sufficient to promote M2 polarization in vivo. Moreover, RNA-sequencing (RNA-seq) confirmed the lack of increased expression of markers of M2 polarization in microglia exposed to CSF1 over-expression, but did reveal changes in expression of other immune related genes. Although treatment with inhibitors of the CSF1 receptor, CSF1R, has been shown to impact other glia, no increased expression of astrocyte or oligodendrocyte lineage markers was observed in CSF1 OE mice. Our data indicate that CSF1 overexpression as an isolated stimulus has limited impacts in the CNS, and that microglia ultimately adapt to the presence of the CSF1 mitogenic signal.

2020-12-01 | GSE151698 | GEO

Interactions in CSF1-driven Tenosynovial Giant Cell Tumors

Project description:A major component of cells in Tenosynovial Giant Cell Tumor (TGCT) consists of bystander macrophages responding to CSF1 that is overproduced by a small number of neoplastic cells with a chromosomal translocation involving the CSF1 gene. An autocrine loop was postulated where the neoplastic cells are stimulated through CSF1R expressed on their surface. Here we use single cell RNA sequencing to investigate cellular interactions in TGCT.

2022-10-01 | GSE210750 | GEO

The effect of a novel form of macrophage colony-stimulating factor (CSF1-Fc) on gene expression in the liver.

Project description:Treatment of mice with daily injections of CSF1-Fc produce a 50% increase in the size of the liver within 5 days. There was extensive proliferation of hepatocytes, similar to that seen following partial hepatectomy. Comparative gene expression profiles of the treated and control livers, alongside macrophages grown in CSF1, indicate extensive infiltration by macrophages in response to CSF1-Fc, and demonstrate that infiltrating macrophages produced several candidate mediators of hepatocyte proliferation.

2013-12-31 | E-GEOD-52636 | biostudies-arrayexpress

A multiplexed single-cell CRISPR screening platform enables systematic dissection of the unfolded protein response

Project description:Functional genomics efforts face tradeoffs between number of perturbations examined and complexity of phenotypes measured. We bridge this gap with Perturb-seq, which combines droplet-based single-cell RNA-seq with a strategy for barcoding CRISPR-mediated perturbations, allowing many perturbations to be profiled in pooled format. We applied Perturb-seq to dissect the mammalian unfolded protein response (UPR) using single and combinatorial CRISPR perturbations. A genome-scale CRISPR interference (CRISPRi) screen identified genes whose depletion perturbs ER homeostasis. Subjecting ~100 hits to Perturb-seq enabled high-precision functional clustering of genes. Single-cell analyses revealed epistasis among the three UPR branches, bifurcated UPR branch activation between cells subject to the same perturbation, and differential activation of the branches across hits, including a feedback loop between the translocon and the IRE1α branch. These studies provide insight into how the three sensors of ER homeostasis monitor distinct types of stress and highlight the ability of Perturb-seq to dissect complex cellular responses.

2016-12-15 | GSE90546 | GEO

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