E-GEOD-36176
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA152915
PROVIDER: E-GEOD-36176 | ExpressionAtlas | 2025-01-24
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-36176-analysis-methods.tsv | Tabular | |||
| E-GEOD-36176-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-36176-configuration.xml | Xml | |||
| E-GEOD-36176-percentile-ranks.tsv | Tabular | |||
| E-GEOD-36176.condensed-sdrf.tsv | Tabular |
Items per page: 5 1 - 5 of 105 |
Similar Datasets
Project description:Gene expression arrays on lung cancer cells exposed to Notch inhibitor
| PRJNA152915 | ENA
Project description:This randomized phase I/II clinical trial is studying the side effects and best dose of gamma-secretase/notch signalling pathway inhibitor RO4929097 when given together with vismodegib and to see how well they work in treating patients with advanced or metastatic sarcoma. Vismodegib may slow the growth of tumor cells. Gamma-secretase/notch signalling pathway inhibitor RO4929097 may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth. Giving vismodegib together with gamma-secretase/notch signalling pathway inhibitor RO4929097 may be an effective treatment for sarcoma.
| 2091475 | ecrin-mdr-crc
Project description:<p>The purpose of the study was to compare gene expression profiles from a cohort of crizotinib-resistant ALK-rearranged lung tumors and a cohort of treatment-naive ALK-rearranged lung tumors. Expression profiles were generated by RNA-seq. In parallel, gene expression profiles were obtained from ALK-rearranged lung cancer cell lines in the presence or absence of the ALK inhibitor TAE684. Gene expression profiles were also obtained from ALK-rearranged cells ectopically expressing genes associated with ALK inhibitor resistance that were identified from a functional genetic study.</p>
| phs000855 | dbGaP
Project description:Non-small cell lung cancer (NSCLC) is the most lethal and prevalent type of lung cancer. In almost all types of cancer, the levels of polyamines (putrescine, spermidine, and spermine) are increased, playing a pivotal role in tumor proliferation. Indomethacin, a non-steroidal anti-inflammatory drug, increases the abundance of an enzyme termed spermidine/spermine-N1-acetyltransferase (SSAT) encoded by the SAT1 gene. This enzyme is a key player in the export of polyamines from the cell. The aim of this study was to compare the effect of indomethacin on two NSCLC cell lines, and their combinatory potential with polyamine-inhibitor drugs in NSCLC cell lines. A549 and H1299 NSCLC cells were exposed to indomethacin and evaluations included SAT1 expression, SSAT levels, and the metabolic status of cells. Moreover, the difference in polyamine synthesis enzymes among these cell lines as well as the synergistic effect of indomethacin and chemical inhibitors of the polyamine pathway enzymes on cell viability were investigated. Indomethacin increased the expression of SAT1 and levels of SSAT in both cell lines. In A549 cells, it significantly reduced the levels of putrescine and spermidine. However, in H1299 cells, the impact of treatment on the polyamine pathway was insignificant. Also, the metabolic features upstream of the polyamine pathway (i.e., ornithine and methionine) were increased. In A549 cells, the increase of ornithine correlated with the increase of several metabolites involved in the urea cycle. Evaluation of the levels of the polyamine synthesis enzymes showed that ornithine decarboxylase is increased in A549 cells, whereas S-adenosylmethionine-decarboxylase and polyamine oxidase are increased in H1299 cells. This observation correlated with relative resistance to polyamine synthesis inhibitors eflornithine and SAM486 (inhibitors of ornithine decarboxylase and S-adenosyl-L-methionine decarboxylase, respectively), and MDL72527 (inhibitor of polyamine oxidase and spermine oxidase). Finally, indomethacin demonstrated a synergistic effect with MDL72527 in A549 cells and SAM486 in H1299 cells. Collectively, these results indicate that indomethacin alters polyamine metabolism in NSCLC cells and enhances the effect of polyamine synthesis inhibitors, such as MDL72527 or SAM486. However, this effect varies depending on the basal metabolic fingerprint of each type of cancer cell.
2021-02-08 | MTBLS873 | MetaboLights
Project description:A collection of cell-type specific constraint-based metabolic models of Calu-3 cells (a human lung epithelial cancer cell line) infected with SARS-CoV-2 based that were generated based on gene-expression data.
2025-04-14 | MODEL2311070005 | BioModels
Project description:Radiotherapy, a treatment modality received by more than half of all cancer patients, remains one of the most effective approaches to achieve local tumour control. Despite increased accuracy driven by technological advances, healthy tissue injury due to off-target radiation exposure can still occur. In this study, we sought to understand the biological effect of radiation-mediated injury to the lung in the context of cancer metastasis, since we had previously reported that tissue regeneration is a feature of the metastatic microenvironment of this organ. We have exposed healthy mouse lung tissue to radiation prior to the induction of metastasis and observed a strong enhancement of cancer cell growth. Lung tissue was preconditioned into a profoundly tumour-supportive microenvironment governed by enhanced regenerative Notch signalling. Most importantly, we found that locally activated neutrophils were key drivers of these tissue perturbations, significantly increasing the metastatic proficiency of irradiated lung tissue and endowing arriving cancer cells with an augmented stemness phenotype. We show that by preventing neutrophil-dependent Notch activation in the irradiated tissue, we were able to significantly offset the radiation-enhanced metastases. Mechanistically, we identified the release of neutrophil granules as the effectors of the pro-tumorigenic preconditioning of the irradiated lung tissue. These findings not only reveal a novel tumour-supportive function of neutrophils in the context of tissue-injury, but also have important clinical implications by suggesting targeting their activity could maximise the success of radiotherapy for the treatment of cancer.
2021-12-13 | PXD027628 | Pride
Project description:Control (DMSO 0.1%; v/v) and 10 M DRB18 were used to treated 5 million A549 lung cancer cells in vitro for 48 hours. The untargeted metabolomics analysis was performed on the cell lysates. The main objective of the study was to determine changes in metabolite abundances in lung cancer after treatment with DRB18, an inhibitor of glucose transporter proteins.
2021-02-15 | MSV000086879 | GNPS
Project description:Cell and protein arrays have demonstrated remarkable utility in the high-throughput evaluation of biological responses; however, they lack the complexity of native tissue and organs and cannot replicate the environment of mature normal or diseased tissues. Here, we describe the development of tissue and organ extracellular matrix (ECM) arrays for screening biological outputs and systems analysis. Tissues and organs were chemically and mechanically processed and then formulated as particles without any enzymatic breakdown. The tissue ECM particles were spotted as two-dimensional tissue ECM arrays or incorporated with cells to generate three-dimensional cell-ECM microtissue arrays, and these methods were compatible with tissues prepared with varied processing techniques. The physical and biochemical properties, including the proteomic composition, of the tissue ECM arrays were characterized and compared with native tissues. The 2D arrays were validated through quantitative analysis of tissue-specific biological outputs of cell matrix production, cell adhesion and proliferation, and cell shape following culture with stem cells, cancer cells, and macrophages. Tissue-specific stem cell osteogenic differentiation on the arrays was comparable between 2D and 3D ECM environments, and revealed lung as an unexpected promoter of osteogenesis. Further gene ontology analysis of lung tissue ECM proteomics showed enrichment for families of proteins associated with skeletal development and osteogenesis. Stem cell biological outputs, along with cancer line adhesion and macrophage shape, were correlated with tissue proteomics, and network analysis identified several protein determinants of cell function. Our methodology enables broad screening of tissue and organ ECMs to connect tissue-specific composition with biological responses via systems analysis, providing a new resource for research and translation.
2015-09-28 | PXD002571 | Pride
Project description:We were interested in characterizing the transcriptional changes that occur on a genome-wide scale following treatment of EGFR-mutant lung cancer cells with targeted therapies. HCC827 human lung cancer cells harboring an amplified EGFR allele with an activating in frame deletion of 15 nucleotides in exon 19 were treated in triplicate with 1uM erlotinib (EGFR inhibitor), AZD-6244 (MEK inhibitor) or BEZ-235 (PI3-Kinase/mTOR inhibitor) for 6 hours, followed by total mRNA isolation and whole transcriptome analysis using Affymetrix U133 Plus 2.0 expression arrays.
2015-02-25 | E-GEOD-51212 | biostudies-arrayexpress