Project description:To seek if ionizing radiation have different biological effect on lung normal cells and cancer cells, we treated lung epithelial cell line BEAS-2B, non-small cell lung cancer cell line A549 and small cell lung cancer cell line H446 with 10 Gy X-ray radiation
Project description:Cell Line: This experiment was designed to measure the transcriptional responses to four kinase inhibitors across a five-logarithm dose range. The A549 human lung cancer cell line was treated with dasatinib, imatinib or nilotinib (4 hours and 20 hours) or PD0325901 (4 hours). Treatments used a 12-point dose range (30 uM with 3-fold dilutions down to 0.17 nM; 0.5% DMSO vehicle for all treatments). Experimental design prevented row or column handling effects being confounded with dose effect.
Project description:Strongly induction of FOSB was observed in a cationic anticancer peptide TP4 treated human A549 lung cancer cell-line, causing obvious cell death. This work aims to address the gene expression profiling upon FOSB overexpression in A549 cell.
Project description:Anticancer drug sagopilone in lung cancer line A549. We performed gene expression analysis of lung cancer cell line A549 treated with sagopilone and paclitaxel. The aim was to analyse gene expression differences between the two drugs in two different concentrations. A549 cells were treated with medium containing either 2.5 nM sagopilone, 40 nM sagopilone, 4 nM paclitaxel or 40 nM paclitaxel, respectively, vehicle (ethanol 0.1%), or were left untreated for 18 hours. The two different concentrations were chosen according the phenotypes they have caused in A549 cells. Treatment with 2.5 nM sagopilone, 4 nM paclitaxel induced an aneuploid cell population, whereas treatment with 40 nM sagopilone and 40 nM paclitaxel induced mitotic arrest.
Project description:Aberrant TGFbeta signalling is a hallmark of epithelial derived tumours. Signalling patterns can depend on the membrane trafficking and internalization of the TGFbeta receptors. Protein kinase C (PKC), particularly the atypical PKC isoforms, alter the trafficking of TGFbeta receptors and can alter TGFbeta induced gene expression. We used microarrays to detail the programme of gene expression underlying TGFbeta induction between control or aPKC silenced A549 cells. Control or aPKC silenced A549 cells were serum starved and treated with TGFbeta for 1 hour. Total RNA was extracted from untreated or TGFbeta treated cells after 8 and 24 hours and analyzed using Affymetrix microarrays. We sought to assess TGFbeta gene expression in aPKC silenced lung cancer cells, as we found that knockdown of aPKC extends TGFbeta signalling as assessed by phospho Smad2 levels. Furthermore, increased expression and oncogenic activity of aPKC (PKCiota) has been reported in lung cancer cells.
Project description:This study reports a screen to identify putative inhibitors of the eIF4F complex for potential effects on blocking coronavirus replication, using HCoV-OC43 (OC43) infection of Vero E6 cells and the lung epithelial cancer line A549 as models.
Project description:This study reports a screen to identify putative inhibitors of the eIF4F complex for potential effects on blocking coronavirus replication, using HCoV-OC43 (OC43) infection of Vero E6 cells and the lung epithelial cancer line A549 as models.
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:Cholesterol treated lung cancer cell A549
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.
