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Homo sapiens

ABSTRACT: A Mechanistic Analysis of the Role of Pro-inflammatory Cytokines in Induction of Epithelial to Mesenchymal Transition in Hepatocellular Carcinoma

PROVIDER: PRJNA395629 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5867972_1.fastq.gz	Fastqsanger.gz
	SRR5867972_2.fastq.gz	Fastqsanger.gz
	SRR5867973_1.fastq.gz	Fastqsanger.gz
	SRR5867973_2.fastq.gz	Fastqsanger.gz
	SRR5867974_1.fastq.gz	Fastqsanger.gz

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Pro-Inflammatory Cytokines Mediate the Epithelial-to-Mesenchymal-Like Transition of Pediatric Posterior Fossa Ependymoma

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Analyzing small RNA sequences from canine stem cell-derived extracellular vesicles primed with TNF-α and IFN-γ

Project description:Acute lung injury is an acute inflammation disorder that disrupts the lung endothelial and epithelial barriers. In this study, we investigated the extracellular vesicles (EVs) obtained via priming inflammatory cytokines such as tumor necrosis factor (TNF)-α and interferon (IFN)-γ on canine adipose mesenchymal stem cells in improving their anti-inflammatory and/or immunosuppressive potential, and/or their ability to alleviate lipopolysaccharide-induced lung injury in vitro. We also explored the correlation between epithelial-to-mesenchymal transition and the inflammatory repressive effect of primed EVs. Using small RNA-Seq, we confirmed that miR-16 and miR-502 significantly increased in EVs from TNF-α and IFN-γ-primed canine adipose mesenchymal stem cells. The pro and anti-inflammatory cytokines were analyzed in a lipopolysaccharide-induced lung injury model and we found that the EV anti-inflammatory effect improved on priming with inflammatory cytokines. EVs obtained from primed stem cells effectively suppress endothelial-to-mesenchymal transition in a lung injury model. Our results suggest a potential therapeutic approach utilizing EVs obtained from adipose mesenchymal stem cells primed with TNF-α and IFN-γ against lung inflammation and endothelial to mesenchymal transition.

2025-06-09 | GSE267973 | GEO

Expression Data from Allogeneic Human Mesenchymal Stem Cells and Primary Cultures of Human Alveolar Epithelial Type II Cells

Project description:Acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) is a severe syndrome affecting more than 200,000 patients annually in the U.S. New studies are needed to understand the biological and clinical mechanisms that impair alveolar epithelial function. Also, innovative therapies are needed for the resolution of pulmonary edema in ARDS. We and other investigators have reported that bone marrow derived mesenchymal stem cells (MSCs) are effective in preclinical models of ALI due to their ability to secrete several paracrine factors that can regulate lung endothelial and epithelial permeability, including growth factors, anti-inflammatory cytokines, and antimicrobial peptides. So in this study we will test the therapeutic value of human MSCs in an in vitro model of acute lung injury induced by pro-inflammatory cytokines. We will identify differentially expressed genes in primary cultures of human alveolar epithelial type II cells and human bone marrow derived mesenchymal stem cells using Affymetrix gene expression arrays. Human mesenchymal stem cells (MSCs) and human alveolar epithelial type II cells were co-cultured in a transwell system. The cells were stimulated with cytomix (a combination of different pro-inflammatory cytokines) under different conditions. Cells were harvested for Affymetrix gene expression arrays. Total 25 samples are analyzed, 3~5 replicates are included.

2015-07-08 | E-GEOD-68610 | biostudies-arrayexpress

Pro-Inflammatory Cytokines Mediate the Epithelial-to-Mesenchymal-Like Transition of Pediatric Posterior Fossa Ependymoma (single-nucleus ATAC-seq)

Project description:Pro-Inflammatory Cytokines Mediate the Epithelial-to-Mesenchymal-Like Transition of Pediatric Posterior Fossa Ependymoma (single-nucleus ATAC-seq)

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Pro-Inflammatory Cytokines Mediate the Epithelial-to-Mesenchymal-Like Transition of Pediatric Posterior Fossa Ependymoma (single-nucleus RNA-seq)

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scRNA-seq of patient-derived PDAC organoids and matched CAFs

Project description:We established direct three-dimensional (3D) co-cultures of primary PDAC organoids and patient-matched CAFs. Single-cell RNA sequencing was performed for three organoid/CAF pairs in mono- and co-culture to uncover transcriptional changes induced by tumor-stroma interaction. Single-cell RNA sequencing data evidenced induction of a pro-inflammatory phenotype in CAFs in co-cultures. Organoids showed increased expression of genes associated with epithelial-to-mesenchymal transition (EMT) in co-cultures and several potential receptor-ligand interactions related to EMT were identified, supporting a key role of CAF-driven induction of EMT in PDAC chemoresistance.

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Oleanolic acid inhibits epithelial–mesenchymal transition of hepatocellular carcinoma by promoting iNOS dimerization

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Homo sapiens

Project description:Lipocalin-2-mediated downregulation of Twist1 reverses the epithelial-mesenchymal transition in hepatocellular carcinoma

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Project description:ARID1A is frequently mutated in ovarian clear-cell carcinoma (OCCC) and often co-exists with activating mutations of PIK3CA. Although induction of pro-inflammatory cytokines has been observed in this cancer, the mechanism by which the two mutations synergistically activate cytokine genes remains elusive. Here we established an in vitro model of OCCC by introducing ARID1A knock-down and mutant PIK3CA in a normal human ovarian epithelial cell line, which resulted in cell transformation and cytokine gene induction. We demonstrate that loss of ARID1A impairs the recruitment of the Sin3A-HDAC complex, while PIK3CA mutation releases RelA from IkB, leading to cytokine gene activation. We show that an NF-kB inhibitor partly attenuates proliferation of OCCC and improves the efficacy of carboplatin both in cell culture and a mouse model. Our study thus reveals the mechanistic link between ARID1A/PIK3CA mutations and cytokine gene induction in OCCC, and suggests NF-kB inhibition can be a potential therapeutic option.

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Comparison of two hepatocellular cancer cell lines with distinct properties regarding epithelial-mesenchymal transition

Project description:The epithelial to mesenchymal transition (EMT) of malignant hepatocytes is a crucial event in hepatocellular carcinoma (HCC) progression and recurrence. We aimed to establish a human model of EMT to examine drug efficacy and specificity in HCC progression. Human HCC cell populations were characterized by immunofluorescence analysis, migration and invasion assays, array comparative genomic hybridization, whole-genome expression profiling and promoter methylation. Therapeutic agents clinically used against HCC were examined for efficacy by determination of IC50 values. Liver cancer cell lines showed either an epithelial or mesenchymal phenotype of which latter showed strong migratory and invasive abilities in vitro. The common cellular origin of both cell types indicated that mesenchymal HCC cells have been derived from epithelial hepatocytes through EMT in the HCC patient. Drug exposure of mesenchymal HCC cells showed higher resistance to the targeted therapeutic agents sorafenib and erlotinib as compared to epithelial HCC cells, which were slightly more resistant to cytostatic drugs. Most remarkably, combined treatment with doxorubicin and sorafenib caused increased susceptibility of both HCC cell types resulting in enhanced drug efficacy. Taken together, this novel model of human HCC allows to monitor the differential effect of liver cancer progression on drug efficacy in pre-clinical studies. hepatocellular carcinoma cell lines HCC-1.2 and HCC-1.1 cells, referred to as 3p and 3sp cells, respectively, were isolated from one HCC patient as described ( Sagmeister S, Eisenbauer M, Pirker C, et al. New cellular tools reveal complex epithelial-mesenchymal interactions in hepatocarcinogenesis. Br J Cancer 2008;99(1):151-9.). 3p cells of passages 10 to 12 and 3sp cells of passages 7 to 13 are termed 3p early and 3sp early, respectively. 3p cells between passage 71 and 76 and 3sp from passage 72 to 87 were termed 3p late and 3sp late, respectively

2011-11-21 | E-GEOD-26391 | biostudies-arrayexpress

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