E-GEOD-32254
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA147353
PROVIDER: E-GEOD-32254 | ExpressionAtlas | 2025-01-24
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-32254-analysis-methods.tsv | Tabular | |||
| E-GEOD-32254-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-32254-configuration.xml | Xml | |||
| E-GEOD-32254-percentile-ranks.tsv | Tabular | |||
| E-GEOD-32254.condensed-sdrf.tsv | Tabular |
Items per page: 5 1 - 5 of 107 |
Similar Datasets
Project description:Claudin 1 mediates TNFα-induced gene expression and cell migration in human lung carcinoma cells
| PRJNA147353 | ENA
Project description:Most of the gas exchange in the human body is carried out by the lungs, and the physiological activities of the lungs are uninterrupted. Due to the deterioration of the external environment, pulmonary cell lesions are common clinical lung diseases. Mechanical cyclic stretching is one kind of bionic technology to observe lung cancer cells. The A549 cell line is the human lung adenocarcinoma cell line derived from a primary lung tumor. This study investigated the effects of mechanical cyclic stretching on A549 cell activity and gene expression profile. Whereas mechanical cyclic stretching had no significant difference in colony formation and cell migration of A549 cells, the cell invasion increased significantly in A549 cells after stretching. In addition, the microarray data showed that mechanical cyclic stretching altered gene expression, induced inflammation of cells, and activation of Wnt/β-catenin and tumor necrosis factor pathways. More importantly, mechanical cyclic stretching activated the expression of tumor necrosis factor-alpha (TNF-α) protein. Therefore, the increase of cell invasion induced by mechanical cyclic stretching might be associated with the activation of TNF-α in human lung adenocarcinoma cells.
2023-04-07 | GSE214041 | 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:Liver cancer has a high mortality rate. Chronic inflammation is one of the leading causes of hepatocellular carcinoma. Recent studies suggested high levels of trimethylamine N-oxide (TMAO) may correlate with increased risk of inflammatory-induced liver cancer. However, the mechanisms by which TMAO promotes liver cancer remain elusive. Here, we established a model of inflammatory-induced liver cancer by treating Hepa1-6 cells with TNF-α. TMAO synergistically increased the proliferation, migration and invasion of Hepa1-6 cells in the presence of TNF-α. We conducted bulk RNA-Seq of the TMAO-treated cell model of inflammatory Hepatocellular carcinoma (HCC)
2022-01-18 | GSE193557 | GEO
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:Idiopathic pulmonary fibrosis (IPF) is associated with the accumulation of collagen-secreting fibroblasts and myofibroblasts in the lung parenchyma. Many mechanisms contribute to their accumulation, including resistance to apoptosis. In previous work, we showed that exposure to the pro-inflammatory cytokines, TNF-α and IFN-γ reverses fibroblast resistance to apoptosis. The goal of this study was to investigate the underlying mechanism. Based on an initial interrogation of the transcriptomes of unstimulated and TNF-α and IFN-γ-stimulated primary lung fibroblasts and the lung fibroblast cell line, MRC5, we show here that among Fas-signaling pathway molecules, Fas expression was increased ~6-fold in an NF-κB and p38mapk-dependent fashion. Prevention of the increase in Fas expression using Fas siRNAs blocked the ability of TNF-α and IFN-γ to sensitize fibroblasts to Fas ligation induced-apoptosis; while enforced adenovirus-mediated Fas overexpression was sufficient to overcome basal resistance to Fas-induced apoptosis. Examination of lung tissues from IPF patients revealed low to absent staining of Fas in fibroblastic cells of fibroblast foci. Collectively, these findings suggest that increased expression of Fas is necessary and sufficient to overcome the resistance of lung fibroblasts to Fas-induced apoptosis. They also suggest that approaches aimed at increasing Fas expression by lung fibroblasts and myofibroblasts may be therapeutically relevant. To investigate the mechanism by which TNF-α and IFN-γ reprogram fibroblasts from resistance to sensitivity to Fas-ligation-induce apoptosis, we exposed human primary lung fibroblasts from an IPF patient (FS087) and non-disease control subject (N78) and the human fetal lung fibroblast cell lung (MRC-5) to TNF-α (10 ng/ml) and IFN-γ (50 U/ml) for 36 hr and analyzed changes in their transcriptomes using Affymetrix microarrays.
2011-01-13 | E-GEOD-26594 | biostudies-arrayexpress
Project description:We have studied the anti-cancer activities of antofine N-oxide isolated and purified from the medicinal plant Cynanchum vincetoxicum. The compound displays a strong cytotoxic effect on several solid tumor cell lines (glioblastoma, breast carcinoma and lung carcinoma) and on T-cell leukemia. It induces cytostasis in the solid tumor cell lines whereas it causes apoptotic cell death in the leukemia cell line. The cytotoxic effect is much weaker in non-cancer control cells. A microarray analysis of the gene expression after a short treatment showed a set of differentially expressed genes in the two types of cancer cells (apoptosis versus cytostasis). Interestingly, a number of genes of the TNF-alpha signaling pathway are up-regulated in the three solid tumor cell lines, including TNF-alpha which is among the most significantly up-regulated genes. The increased TNF-alpha, TNFAIP3 and BIRC3 mRNA levels were further confirmed after different treatment durations by real-time quantitative PCR (qPCR). Our results suggest that inhibition of cell proliferation in solid tumor cells essentially occurs through TNF-alpha signaling whereas no conclusion could be drawn concerning the pathways leading to apoptotic cell death in leukemia cells due to the reduced number of differentially expressed genes.ﾔ
2014-09-23 | E-MTAB-1900 | 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:Background: α-catulin may functions as an oncoprotein, sustaining proliferation by preventing cellular senescence and promoting cancer cell migration. In this study, we investigated the mechanism of α-catulin in cancer cell migration and metastasis in lung cancer. Method: α-catulin mRNA expression was isolated from A549/AS2neo (control) and A549/AS2neo-α-catulin stable cells. The Phalanx Human OneArray microarray analysis was performed to identify α-catulin downstream genes. Results: Overexpression of α-catulin increased cancer cell migration and metastasis. By using Phalanx Human OneArray microarray we have identified panel of genes altered by α-catulin overexpression, consisting of CDC42, intergrins and genes related to cytoskeleton remodeling. Conclusion: α-catulin is an oncoprotein and promotes lung cancer cell migration and metastasis.
2012-08-16 | GSE40141 | GEO
Project description:The tumor evolution model posits that malignant transformation is preceded by randomly distributed driver mutations in cancer genes, which cause clonal expansions in phenotypically normal tissues. Although clonal expansions can remodel entire tissues1-3, the mechanisms behind why only a small number of clones transform into malignant tumors remain enigmatic. Here, we develop an in vivo single-cell CRISPR strategy to systematically investigate tissue-wide clonal dynamics of the 150 most frequently mutated squamous cell carcinoma genes. We couple ultrasound-guided in utero lentiviral microinjections, single-cell RNA sequencing and guide capture to longitudinally monitor clonal expansions and document their underlying gene programs at single-cell transcriptomic resolution. We uncover a TNF-α signaling module, dependent on TNF receptor 1 and involving macrophages, that acts as a generalizable driver of clonal expansions in epithelial tissues. Conversely, during tumorigenesis, the TNF-α signaling module is downregulated. Instead, we identify a subpopulation of invasive cancer cells that switch to an autocrine TNF-α gene program, associated with epithelial-mesenchymal transition. Finally, we provide in vivo evidence that the autocrine TNF-α gene program is sufficient to mediate invasive properties and show that the TNF-α signature correlates with shorter overall survival in human squamous cell carcinoma patients. Collectively, our study demonstrates the power of applying in vivo single-cell CRISPR screening to mammalian tissues, unveils distinct TNF-α programs in tumor evolution and highlights the importance of understanding the relationship between clonal expansions in epithelia and tumorigenesis.
2024-07-17 | GSE235325 | GEO