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
2015-08-17 | 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:Human lung squamous cell carcinoma expression profiling
| PRJNA118343 | 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:Claudin proteins are major constituents of epithelial and endothelial tight junctions (TJ), where they serve as regulators of paracellular permeability to ions and solutes. Claudin-18, a member of the large claudin family, is highly expressed in lung epithelium. To elucidate the role of claudin-18 in alveolar epithelial barrier function and fluid homeostasis, we generated claudin-18 knockout (C18 KO) mice. Increased alveolar fluid clearance (AFC) observed in C18 KO mice may have accounted for absence of lung edema despite increased alveolar solute permeability compared to wild type (WT) controls. Higher AFC in C18 KO mice was associated with higher Na-K-ATPase activity and increased expression of the Na-K-ATPase β1 subunit compared to WT controls. Consistent with in vivo findings, alveolar epithelial cell (AEC) monolayers derived from C18 KO mice exhibited lower transepithelial electrical resistance (RT) accompanied by increased solute and ion permeability without changes in ion selectivity. Expression of claudin-3 and claudin-4 was markedly increased in whole lung and in freshly isolated AEC from C18 KO mice, while claudin-5 was unchanged. In contrast, occludin, another major component of the TJ complex, was significantly decreased in C18 KO lung. Further analysis revealed rearrangements in the F-actin cytoskeleton in C18 KO MAECM. These findings demonstrate a crucial non-redundant role for claudin-18 in regulation of alveolar epithelial tight junction composition and permeability to ions and solutes. Importantly, increased AFC in C18 KO mice identifies additional roles for claudin-18 in alveolar fluid homeostasis beyond its direct contributions to barrier properties of the alveolar epithelium. Animals with a ubiquitous knockout (C18 KO) were obtained by crossing mice harboring a conditional (floxed) allele of claudin-18 (Cldn18F/F) with CMV-cre deleter mice to delete exons 2 and 3 by Cre/loxP recombination.
2014-04-06 | E-GEOD-48443 | biostudies-arrayexpress
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:Claudin proteins are major constituents of epithelial and endothelial tight junctions (TJ), where they serve as regulators of paracellular permeability to ions and solutes. Claudin-18, a member of the large claudin family, is highly expressed in lung epithelium. To elucidate the role of claudin-18 in alveolar epithelial barrier function and fluid homeostasis, we generated claudin-18 knockout (C18 KO) mice. Increased alveolar fluid clearance (AFC) observed in C18 KO mice may have accounted for absence of lung edema despite increased alveolar solute permeability compared to wild type (WT) controls. Higher AFC in C18 KO mice was associated with higher Na-K-ATPase activity and increased expression of the Na-K-ATPase β1 subunit compared to WT controls. Consistent with in vivo findings, alveolar epithelial cell (AEC) monolayers derived from C18 KO mice exhibited lower transepithelial electrical resistance (RT) accompanied by increased solute and ion permeability without changes in ion selectivity. Expression of claudin-3 and claudin-4 was markedly increased in whole lung and in freshly isolated AEC from C18 KO mice, while claudin-5 was unchanged. In contrast, occludin, another major component of the TJ complex, was significantly decreased in C18 KO lung. Further analysis revealed rearrangements in the F-actin cytoskeleton in C18 KO MAECM. These findings demonstrate a crucial non-redundant role for claudin-18 in regulation of alveolar epithelial tight junction composition and permeability to ions and solutes. Importantly, increased AFC in C18 KO mice identifies additional roles for claudin-18 in alveolar fluid homeostasis beyond its direct contributions to barrier properties of the alveolar epithelium.
2014-04-06 | GSE48443 | 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