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Unknown,Transcriptomics,Genomics,Proteomics

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Cross species hybridization of human cancer cells xenografted into different mouse organ sites

ABSTRACT: To test gene expression changes of human cancer cells and mouse surrounding tissue cells during tumor progression, 4 different types of cancer cells (MDA-MB231Br3, PC14Br4, KM12M, A375SM) were injected into mouse brain, skin and orthotopic sites. RNAs containing human cancer cells and mouse surrounding tissue cells were extracted and hybridized into human and mouse arrays at the same times and it revealed the brain microenvironment induced complete reprogramming of metasized cancer cells, resulting in a gain of neuronal cell characteristic , mimicking neurogenesis during development. Human in vivo: 4 KB, 4 KS, 3 KC, 5 MB, 5 MF, 4 MS, 3 PB, 3 PL, 4 PS, 5 AB, 5 AS , 1 BR_N_PC Mouse in vivo: 4 KB, 4 KS, 3 KC, 5 MB, 5 MF, 4 MS, 3 PB, 3 PL, 4 PS, 5 AB, 5 AS , 3 BR, 3 PC_BRM, 1 BR_PCM

ORGANISM(S): Mus musculus

SUBMITTER: Sangbae Kim

PROVIDER: E-GEOD-19184 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:WC/KC/KS

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Infiltrating monocyte-derived macrophages and resident kupffer cells display different ontogeny and functions in acute liver injury

Project description:Molecular profiling of infiltrating monocyte-derived macrophages versus resident kupffer cells following acute liver injury The liver has a remarkable capacity to regenerate after injury; yet, the role of macrophages (MF) in this process remains controversial mainly due to difficulties in distinguishing between different MF-subsets. Here, we utilized a murine model of acute liver injury caused by overdose of acetaminophen (APAP) and defined three distinct MF subsets that populate the liver following injury. Accordingly, resident Kupffer cells (KC) were significantly reduced upon APAP-challenge and started recovering by self-renewal at resolution phase without contribution of circulating Ly6Chi monocytes. The latter were recruited in a CCR2 and M-CSF mediated pathway at the necro-inflammatory phase and differentiated into ephemeral Ly6Clo MF subset at resolution phase. Moreover, their inducible ablation resulted in impaired recovery. Microarray based molecular profiling uncovered high similarity between steady state KC and those recovered at the resolution phase. In contrast, KC and monocyte-derived MF displayed distinct pro-restorative genetic signature at the resolution phase. Finally, we show that infiltrating monocytes acquire a pro-restorative polarization manifested by unique expression of pro-angiogenesis mediators and genes involved with inhibition of neutrophil activity and recruitment and promotion of their clearance. Collectively, our results present a novel phenotypic, ontogenic and molecular definition of liver-MF compartment following acute injury. 11 Samples (arrays) were performed. We generated pairwise comparison between all the different macrophages stages, using Partek Genomics Suite. Genes with p?5%[FDR] and a fold-change difference of ?2 or <-2 were selected.

2014-08-01 | E-GEOD-55606 | biostudies-arrayexpress

Infiltrating monocyte-derived macrophages and resident kupffer cells display different ontogeny and functions in acute liver injury

2014-08-01 | GSE55606 | GEO

Heterogeneity effects of nanoplastics and lead on zebrafish intestine identified by single-cell sequencing

Project description:Plastic particles in water environment can adsorb heavy metals, leading to combined toxicity to aquatic organisms. However, current conclusions are mostly obtained based on cell population-average responses. Heterogeneity effects among cell populations in aquatic organisms remain unclear. This study analyzed the heterogeneity effects of 200 μg/L 100 nm polystyrene nanoplastics (PS-NPs), 50 μg/L lead (Pb), and their combined exposures on zebrafish intestine cells by single-cell RNA sequencing.A total of 38640 cells in the zebrafish intestine was obtained and identified as seven cell populations, including enterocytes, macrophages, neutrophils, B cells, T cells, enteroendocrine cells, and goblet cells.Co-exposure of PS-NPs and Pb caused similar transcriptome profiles with PS-NPs exposure in macrophages, which changed immunological recognition processes. The Pb exposure influenced the macrophages by direct cytotoxicity. However, the Pb alone and combined exposures induced similar modes of action in the enterocytes, including the generation of oxidative stress and abnormal lipid metabolism.

2022-02-25 | GSE165888 | GEO

Gene expression data from CD34+ BMMCs/PBMCs from JAK2V617F positive MPN patients vs. Healthy controls

Project description:Philadelphia chromosome-negative myeloproliferative neoplasms (MPN) consist of primary myelofibrosis (PMF), polycythemia vera (PV), essential thrombocythemia (ET) and seconday myelofibrosis (pPV-MF or pET-MF) In this dataset, we compare the gene expression data of bone marrow (BM) or peripheral blood (PB) mononuclear cells of CD34+ cells from JAK2V617F mutated patients vs. healthy donors

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AR variant ARv567es induces carcinogenesis in a novel transgenic mouse model of prostate cancer.

Project description:Androgen deprivation therapy remains the primary treatment modality for patients with metastatic prostate cancer but is uniformly marked by progression to castration-resistant prostate cancer (CRPC) after a period of regression. Continued activation of androgen receptor (AR) signaling is attributed as one of the most important mechanisms underlying failure of therapy. Recently, the discovery of constitutively active AR splice variants (AR-Vs) adds more credence to this idea. Expression of AR-Vs in metastases portends a rapid progression of the tumor. However, the precise role of the AR-Vs in CRPC still remains unknown. ARv567es is one of the two AR variants frequently found in human CRPC xenografts and metastases. Herein, we developed a probasin (Pb) promoter-driven ARv567es transgenic mouse, Pb-ARv567es, to evaluate the role of ARv567es in both autonomous prostate growth and progression to CRPC. We found that expression of ARv567es in the prostate results in epithelial hyperplasia by 16 weeks and invasive adenocarcinoma is evident by 1 year of age. The underlying genetic cellular events involved a cell cycle-related transcriptome and differential expression of a spectrum of genes that are critical for tumor initiation and progression. These findings indicate that ARv567es could induce tumorigenesis de novo and signifies the critical role of AR-Vs in CRPC. Thus, the Pb-ARv567es mouse could provide a novel model in which the role of AR variants in prostate cancer progression can be examined. Custom Agilent 44K whole mouse genome expression oligonucleotide microarrays were used to profile prostate tissue from probasin (Pb) promoter-driven ARv567es transgenic mice and control littermates. Total RNA was isolated and amplified prior to hybridization against a common reference pool of normal adult mouse tissues.

2014-09-11 | E-GEOD-61303 | biostudies-arrayexpress

Spatiotemporally-resolved mapping of RNA binding proteins via functional proximity labeling reveals a mitochondrial mRNA anchor that promotes stress recovery

Project description:We develop a method to enrich subcompartment-specific RNA binding proteins (RBPs) by combining peroxidase-catalyzed PL with organic-aqueous phase separation of crosslinked protein-RNA complexes (APEX-PS).

2021-03-18 | MSV000087070 | MassIVE

RNA profiling of PB-020 and anti-PD-1 antibody treated MC38 tumor tissue

Project description:Immune surveillance escaping is essential for survival of original tumor. Considering PB-020’s good pharmacokinetic properties, combined effect of PB-020 and immunotherapy drugs is worth studying. As PB-020 can effectively suppress mouse colorectal cancer cell lines in cell culture, we tested the effect of combining PB-020 with the anti-PD-1 monoclonal antibody RMP1-14 on the growth of subcutaneously implanted MC38 cells to C57BL/6 mice as a syngeneic mouse model of colorectal cancer. To clarify the molecular mechanism underling this anti-cancer therapy, we executed RNA sequencing of tumor sample obtained from the experiment above.

2022-12-14 | GSE189469 | GEO

Deficient Endoplasmic Reticulum-Mitochondrial Phosphatidylserine Transfer Causes Liver Disease

Project description:Non-alcoholic fatty liver is the most common liver disease worldwide. Here, we show that the mitochondrial protein mitofusin 2 (Mfn2) protects against liver disease. Reduced Mfn2 expression was detected in liver biopsies from patients with non-alcoholic steatohepatitis (NASH). Moreover, reduced Mfn2 levels were detected in mouse models of steatosis or NASH, and its re-expression in a NASH mouse model ameliorated the disease. Liver-specific ablation of Mfn2 in mice provoked inflammation, triglyceride accumulation, fibrosis, and liver cancer. We demonstrate that Mfn2 binds phosphatidylserine (PS) and can specifically extract PS into membrane domains, favoring PS transfer to mitochondria and mitochondrial phosphatidylethanolamine (PE) synthesis. Consequently, hepatic Mfn2 deficiency reduces PS transfer and phospholipid synthesis, leading to endoplasmic reticulum (ER) stress and the development of a NASH-like phenotype and liver cancer. Ablation of Mfn2 in liver reveals that disruption of ER-mitochondrial PS transfer is a new mechanism involved in the development of liver disease.

2018-01-25 | MTBLS600 | MetaboLights

Preventive Treatment with a CD73 Small Molecule Inhibitor Enhances Immune Surveillance in K-Ras Mutant Pancreatic Intraepithelial Neoplasia

Project description:Immunoprevention is an emerging consideration for solid tumors, including pancreatic ductal adenocarcinoma (PDAC). We and others have shown that Kras mutations in genetic models of spontaneous pancreatic intraepithelial neoplasia (PanIN), which is a precursor to PDAC, results in CD73 expression in the neoplastic epithelium and some populations of infiltrating immune cells, including macrophages and CD8 T cells. CD73 is an ecto-enzyme that converts extracellular adenosine monophosphate (AMP) to adenosine, a critical immune inhibitory molecule in PDAC. We hypothesized inhibition of CD73 would reduce the incidence of PanIN formation and alter the immune microenvironment. To test our hypothesis, we used the KrasG12D; PdxCre1 (KC) genetically engineered mouse (GEM) model and tested the utility of AB-680, a small molecule inhibitor targeting CD73, to inhibit PanIN progression. AB-680, or vehicle control, was administered using oral gavage delivery three days/week at 10mg/kg, beginning when the mice were two months old and lasting three months. We euthanized the mice at five months old. In the KC model, we quantified significantly less pancreatitis, early and advanced PanIN, and quantified a significant increase in M1 macrophages in AB-680-treated mice. Single Cell RNA sequencing (scRNA-seq) of pancreata of AB-680 treated mice revealed increased infiltration of CD4+ T cells, CD8+ T cells, and mature B cells. The scRNA-seq analysis showed that CD73 inhibition reduced M2 macrophages, acinar, and PanIN cell populations. CD73 inhibition enhanced immune surveillance and expanded unique clonotypes of TCR and BCR, indicating that inhibition of CD73 augments adaptive immunity early in the neoplastic microenvironment.

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