Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA900293 | ENA |
REPOSITORIES: ENA
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Project description:TGFb and/or crizotinib were treated on A549 cell line to understand molecular mechanisms of action of crizotinib in TGF signaling pathway in lung cancer through gene expression profile data.
2022-09-27 | GSE189047 | GEO
Project description:Silver nanoparticles (AgNPs) have shown great potential as therapeutic agents due to their ability to cause apoptotic cell death in cancer cells. However, little knowledge is available regarding the underlying action mechanisms of AgNPs towards multi-drug resistant cancer cells. Herein, we employed quantitative proteomics to investigate the cytotoxic mechanisms of AgNPs on both cisplatin-sensitive (A549 cells) and -resistant (A549/DDP cells) human lung adenocarcinoma and to explore their potential anticancer abilities. We first performed cytotoxicity tests and found that AgNPs exert similar cytotoxic effects on A549 and A549/DDP cells. At the proteome level, A549 and A549/DDP cells responded to AgNPs distinctively and similarly by causing cell apoptosis via upregulating RNA metabolism, suppressing VEGF siganling pathway, repressing p53-mediated pathways, promoting cell cycle arrest, etc. Additionally, AgNPs remarkably induced ROS generation in A549 and A549/DDP cells. The mitotoxicity results further confirmed the effectiveness of AgNPs in hampering mitochondrial function and respiration in A549 and A549/DDP cells. Overall, our investigations showed that AgNPs could effectively induce cell deaths in human lung adenocarcinoma cells regardless of their sensitivities to cisplatin, suggesting that AgNPs could be potentially used in biomedical aspects as an anticancer agent in alleviating the problem of acquired drug resistance in chemotherapy.
2025-05-30 | PXD064272 | Pride
Project description:Resveratrol, a natural phytoestrogen found in red wine and a variety of plants, is reported to have protective effects against lung cancer, however there is very little work directed towards the understanding of the mechanism of action of resveratrol in lung cancer. In this study we used an experimental approach to understand the biological activity and molecular mechanisms of resveratrol in A549 lung cancer cells. Gene expression profiles were compiled using an oligonucleotide microarray to determine altered expression levels in resveratrol treated cells. Keywords: Genetic modification of A549 cells in response to resveratrol
2007-09-15 | GSE9008 | GEO
Project description:Background: Lung cancer is the leading cause of cancer related death worldwide. Over the past 15 years no major improvement of survival rates could be accomplished. The recently discovered histone methyltransferase KMT9 as epigenetic regulator of prostate tumor growth has now raised hopes of enabling new cancer therapies. In this study we aimed to identify the function of KMT9 in lung cancer which has remained elusive so far. Methods: We linked full transcriptome and proteome analyses of A549 lung adenocarcinoma cells using RNA-Seq and mass spectrometry with functional cell culture, real-time proliferation and flow cytometry assays. Results: KMT9 is expressed in lung cancer tissue and cell lineswith high levels of KMT9 correlating with poor patient survival. We identified 460 overlapping genes and proteins that are deregulated upon knock-down of KMT9alpha in A549 cells. These genes cluster with proliferation, cell cycle and cell death gene sets as well as with subcellular organelles in gene ontology analysis. Knock-down of KMT9alpha inhibits lung cancer cell proliferation and induces non-apoptotic cell death in A549 cells. Conclusions: The novel histone methyltransferase KMT9 is crucial for proliferation and survival of lung cancer cells harboring various mutations. Small molecule inhibitors targeting KMT9 therefore should be further examined as potential milestones in modern epigenetic lung cancer therapy.
2020-05-26 | PXD014145 | Pride
Project description:Micropapillary adenocarcinoma (MPC) is an aggressive histologic subtype of lung adenocarcinoma (LUAD). MPC is composed of small clusters of cancer cells exhibiting inverted polarity. However, the mechanism underlying its formation is poorly understood. Here we show that hypoxia is involved in MPC formation. Spatial transcriptome analysis with human LUAD tissue suggested that hypoxia-inducible factor (HIF)-1 signaling is activated in MPC. Hypoxia induced the formation of MPC-like structures (MLSs) with inverted polarity in a three-dimensional culture system using A549 human LUAD cells, and HIF-1α was indispensable for MLS formation. RNA sequencing analysis demonstrated that A549 cells forming MLSs exhibited a gene expression signature similar to that of lung MPC. Moreover, MLS formation enhanced the resistance of A549 cells to natural killer cell cytotoxicity. Our findings suggest that hypoxia drives lung MPC formation through HIF-1α and that immune escape from natural killer cells might underlie the aggressiveness of MPC.
2025-01-08 | GSE240551 | GEO
Project description:Resveratrol, a natural phytoestrogen found in red wine and a variety of plants, is reported to have protective effects against lung cancer, however there is very little work directed towards the understanding of the mechanism of action of resveratrol in lung cancer. In this study we used an experimental approach to understand the biological activity and molecular mechanisms of resveratrol in A549 lung cancer cells. Gene expression profiles were compiled using an oligonucleotide microarray to determine altered expression levels in resveratrol treated cells. Experiment Overall Design: A549 cells were treated with resveratrol (25microM) or with ethanol control for 48 h. 4 samples in all were hybridized to the affymetrix chip, one control sample and 3 replicates of the resveratrol treated sample. Experiment Overall Design: Gene ontology-based gene lists are supplied in a supplementary file (Genelists.txt) at the foot of this record.
2008-06-16 | E-GEOD-9008 | biostudies-arrayexpress
Project description:Comparison of expression profiles detected in A549 cells exposed to DMSO, TCDD, and BaP for 2w Exposure to persistent ligands of aryl hydrocarbon receptor (AhR) has been found to cause lung cancer in experimental animals and lung adenocarcinomas are often associated with enhanced AhR expression and aberrant AhR activation. In order to better understand the action of toxic AhR ligands in lung epithelial cells, we performed global gene expression profiling in order to analyse TCDD- induced changes in A549 transcriptome, and compare them with changes in transcriptome of A549 cells exposed to BaP for 2w.
2019-09-01 | GSE122733 | GEO
Project description:Label-free proteomics and off-target metabolomics were used to investigate the changes in protein and metabolite content before and after trans-delta viniferin treatment, and to explore the possible mechanism of drug action on A549 cells
2020-01-15 | PXD017098 |