Homo sapiens
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-32254
PROVIDER: PRJNA147353 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Claudin 1 mediates TNF alpha-induced gene expression and cell migration in human lung carcinoma cells
2025-01-24 | E-GEOD-32254 | ExpressionAtlas
Project description:Epithelial-mesenchymal transition (EMT) is an important mechanism in carcinogenesis. To determine the mechanisms that are involved in the regulation of EMT is crucial to develop new biomarkers and therapeutic targets towards cancers. In this study, when TGFÃ1 and TNFa were used to induce EMT in human lung carcinoma A549 cells, we were surprised to find an increase in an epithelial cell tight junction marker, Claudin 1. We further identified that it was the TNFa and not the TGFÃ1 that induced the fibroblast-like morphology changes. TNFa also caused the increase in Claudin-1 gene expression and protein levels in Triton X-100 soluble cytoplasm fraction. Down-regulation of Claudin-1, using small interfering RNA (siRNA), inhibited 75% of TNFa-induced gene expression changes. Claudin-1 siRNA effectively blocked TNFa-induced molecular functional networks related to inflammation and cell movement. Wound-healing assay showed that Claudin-1 siRNA was able to significantly reduce TNF-enhanced cell migration. Furthermore, over expression of Claudin 1 with a Claudin 1-pcDNA3.1/V5-His vector enhanced cell migration. In conclusion, these observations indicate that Claudin 1 acts as a critical signal mediator in TNFa-induced gene expression and cell migration in human lung cancer cells. Further analyses of these cellular processes may be helpful in developing novel therapeutic strategies. 4 groups (with or without TNFα, control or Claudin 1 siRNA) of human lung adenocarcinoma A549 cells with 3 replicates per group.
2012-06-12 | E-GEOD-32254 | biostudies-arrayexpress
Project description:Epithelial-mesenchymal transition (EMT) is an important mechanism in carcinogenesis. To determine the mechanisms that are involved in the regulation of EMT is crucial to develop new biomarkers and therapeutic targets towards cancers. In this study, when TGFß1 and TNFa were used to induce EMT in human lung carcinoma A549 cells, we were surprised to find an increase in an epithelial cell tight junction marker, Claudin 1. We further identified that it was the TNFa and not the TGFß1 that induced the fibroblast-like morphology changes. TNFa also caused the increase in Claudin-1 gene expression and protein levels in Triton X-100 soluble cytoplasm fraction. Down-regulation of Claudin-1, using small interfering RNA (siRNA), inhibited 75% of TNFa-induced gene expression changes. Claudin-1 siRNA effectively blocked TNFa-induced molecular functional networks related to inflammation and cell movement. Wound-healing assay showed that Claudin-1 siRNA was able to significantly reduce TNF-enhanced cell migration. Furthermore, over expression of Claudin 1 with a Claudin 1-pcDNA3.1/V5-His vector enhanced cell migration. In conclusion, these observations indicate that Claudin 1 acts as a critical signal mediator in TNFa-induced gene expression and cell migration in human lung cancer cells. Further analyses of these cellular processes may be helpful in developing novel therapeutic strategies.
2012-06-13 | GSE32254 | GEO
Project description:A collection of cell-type specific constraint-based metabolic models of human H1299 cells (human non-small cell lung carcinoma cell line) infected with SARS-CoV-2 based that were generated based on gene-expression data.
2025-04-07 | MODEL2311070004 | BioModels
Project description:Endothelial stromal cells enhance lung-tumor cell migration through TNFα and SDF-1α secretion
| PRJNA179082 | ENA
Project description:This microarray analysis was designed to determine (1) the impact of ERα expression on cellular TNFα response and estrogen-TNFα signaling crosstalk and (2) whether cigarette sidestream smoke particulates had estrogen-like action in human lung adenocarcinoma cells. The lung adenocarcinoma cell line CL1-5(TO-ERα)#18 was used as a model. Expression of ERα in this cell line is under Tet-on regulation and can be induced by addition of doxycycline. For the Objective 1, we found three types of TNFα responsive genes: estrogen/ERα-dependent, estrogen/ERα-enhanced, and estrogen/ERα-independent. For the Objective 2, the microarray data revealed that cigarette sidestream smoke particulates regulated given genes via ERα as 17β-estradiol in lung adenocarcinoma cells. Some of these ERα target genes had been identified previously.
2020-10-07 | GSE67475 | GEO
Project description:Our preliminary studies performed in vitro show that MDA-MB-231-FOXC1 cell, which were used to mimic the lung-colonizing triple-negative breast cancer cells, was an indispensable component for the induction of migration and tube formation of lung endothelial cells. Moreover, our results further show that mouse lung fibroblast-derived chemokines CCL2/7 act on MDA-MB-231-FOXC1 cells, which mediates the migration and tube formation of lung endothelial cells in vitro. To understand the signaling pathways activated by CCL2/7 in MDA-MB-231-FOXC1 cells, we performed RNA-Seq assay.
2019-05-18 | GSE131383 | GEO
Project description:The tumorigenicity of human pluripotent stem cells (hPSCs) is a major safety concern for their application in regenerative medicine. Here we identify the tight-junction protein Claudin-6 as a specific cell surface marker of hPSCs that can be used to selectively remove Claudin-6-positive cells from mixed cultures. We show that Claudin-6 is absent in adult tissues but highly expressed in undifferentiated cells, where it is dispensable for hPSC survival and self-renewal. We use three different strategies to remove Claudin-6-positive cells from mixed populations: an antibody against Claudin-6; a cytotoxin-conjugated antibody that selectively targets undifferentiated cells; and clostridium perfringens enterotoxin, a toxin that binds several Claudins, including Claudin-6, and efficiently kills undifferentiated cells, thus eliminating the tumorigenic potential of hPSC-containing cultures. This work provides a proof of concept for the use of Claudin-6 to eliminate residual undifferentiated hPSCs from culture, highlighting a strategy that may increase the safety of hPSC-based cell therapies. total RNA was isolated from teratomas or from embryoid bodies differentiated from human induced pluripotent stem cells
2013-06-01 | E-GEOD-38088 | biostudies-arrayexpress
Project description:Chronic inflammation plays a significant role in tumor promotion, migration and invasion. Using microarray analysis, we observed a profound increase in genes involved in pro-inflammatory pathways in epidermal growth factor receptor inhibitor (EGFRI)-treated head and neck squamous cell carcinoma (HNSCC) cell lines compared to their respective vehicle-treated cell lines. We hypothesized that the efficacy of EGFRIs may be offset by the pro-inflammatory response that these drugs produce in HNSCC tumor cells. We found that clinical EGFRIs such as erlotinib, cetuximab, lapatinib and panitumumab induced the secretion of pro-inflammatory cytokines such as IL-2, IL-4, IL-6, IL-8, GM-CSF, TNFα and IFNγ. Focusing on IL-6, we found that erlotinib induced a time-dependent increase in IL-6 mRNA and protein expression and exogenous IL-6 was able to protect HNSCC cells from erlotinib-induced cytotoxicity. Conversely, an IL-6 receptor antagonist tocilizumab, sensitized HNSCC cells to erlotinib in vitro and in vivo. Inhibitors of NFκB, p38 and JNK suppressed erlotinib-induced IL-6 expression, suggesting an important role of NFκB and MAPK pathways in IL-6 expression. Furthermore, knockdown of NADPH oxidase 4 (NOX4) suppressed erlotinib-induced pro-inflammatory cytokines expression. Taken together, these results suggest that clinical EGFRIs induce the expression of pro-inflammatory cytokines via NOX4. Therefore, the anti-tumor activity of EGFRIs may be partially reduced by activation of NOX4-mediated pro-inflammatory pathways in HNSCC. Total RNA was isolated from Head and Neck Squamous Cell Carcinoma cell lines FADU, SQ20B and Cal 27 subjected to 48 hours of 0.01% DMSO or 5uM EGFR inhibitor, erlotinib treatment.
2014-04-08 | E-GEOD-45891 | biostudies-arrayexpress
Project description:Here, we investigated the time-course changes in the pattern of microRNA (miRNA) expression of TNFα and IFNγ-stimulated and unstimulated hCMEC/D3 cells, an immortalized human cerebral microvascular endothelial cell line. In order to investigate pro-inflammatory cytokine-induced changes in miRNA levels in hCMEC/D3 cells, we challenged brain endothelial cells with TNFα and IFNγ (100 ng/ml) for 2 h, 6 h and 24 h and determined microRNA expression in cytokine-stimulated and unstimulated cells
2014-04-29 | E-GEOD-44692 | biostudies-arrayexpress