Project description:Senescence in WI-38 cell context was induce by RASv12 over expression Cellular senescence is a permanent cell cycle arrest that is triggered by cancer- initiating or promoting events in mammalian cells and is now considered a major tumour suppressor mechanism. Here, we did a transcriptomic analysis and compared WI-38 contol wich is a human fibroblaste cell line and WI-38 that overexpressed RASv12 a G protein that induce senescence. The goal of our project is to compare transciptomic profile of human growing fibroblast (WI-38 control) and senescent human fibroblast (WI-38 OERAS)
Project description:Senescence in WI-38 cell context was induce by RASv12 over expression Cellular senescence is a permanent cell cycle arrest that is triggered by cancer- initiating or promoting events in mammalian cells and is now considered a major tumour suppressor mechanism. Here, we did a transcriptomic analysis and compared WI-38 contol wich is a human fibroblaste cell line and WI-38 that overexpressed RASv12 a G protein that induce senescence. The goal of our project is to compare transciptomic profile of human growing fibroblast (WI-38 control) and senescent human fibroblast (WI-38 OERAS) Comparaison WI-38 vs WI-38 OE RAS
Project description:microRNA array of 4 cell lines: WI-38 primary fibroblasts (“Control”), slow growers (early passage after immortalization, Slow), fast growers (extensive passaging after immortalization) and fast growers transformed by constitutively activated mutant H-RasV12 (“Ras”)
Project description:A study comparing small extracellular vesicles (sEVs) from WI-38 and A549 cells. The proteome of the two sources of sEVs were compared to find proteins that could distinguish WI-38-derived sEVs from A549-derived sEVs. These protein markers were used as proof-of-principle biomarkers for a FRET-based sEV biomarker assay.
Project description:We have identified through high-throughput screen a number of small molecules that promote resistance of human WI-38 cells to hydrogen peroxide. To look into potential mechanism of action for a chalcone hit, we analyzed transcriptional profile by RNA-seq for WI-38 cells treated with this molecule.
Project description:Cellular responses to carcinogens are typically studied in transformed cell lines, which do not reflect the physiological status of normal tissues. To address this question, we have characterized the transcriptional program and cellular responses of normal human lung WI-38 fibroblasts upon exposure to the ultimate carcinogen benzo[a]pyrene diol epoxide (BPDE). Exposure to BPDE induces a strong inflammatory response in WI-38 primary fibroblasts. Whole-genome microarray analysis shows induction of several genes related to the production of inflammatory factors, including those that encode interleukins (ILs), growth factors, and enzymes related to prostaglandin synthesis and signaling. This is the first demonstration that a strong inflammatory response is triggered in primary fibroblasts in response to a reactive diol epoxide derived from a polycyclic aromatic hydrocarbon.
Project description:microRNA array of 4 cell lines: WI-38 primary fibroblasts (â??Controlâ??), slow growers (early passage after immortalization, Slow), fast growers (extensive passaging after immortalization) and fast growers transformed by constitutively activated mutant H-RasV12 (â??Rasâ??) WI-38 cells were grown in 37° in MEM supplemented with 10% non-heat-inactivated fetal bovine serum (Sigma), pen-strep, sodium pyruvate, L-glutamine solution (Beit HaEmek). RNA was extracted using Nucleospin miRNA kit (Macherey-Nagel), according to manufacturerâ??s instructions. microRNA array analysis was done in duplicates, using the miRNA Complete Labeling and Hyb Kit (Agilent, 5190-0456) according to the manufacturer's instructions. Briefly, for each sample 100ng RNA was dephosphorylated, denatured, labeled with Cyanine 3-pCp and purified using Micro Bio-Spin 6 Columns. Hybridization was done for 20h with Agilent SurePrint G3 Unrestricted miRNA 8x60K (Release 19.0) arrays. Arrays were scanned using an Agilent DNA microarray scanner, and analyzed using the AgiMicroRna package in R with the RMA algorithm. The function filterMicroRna was applied with the following parameters: control = TRUE, IsGeneDetected = TRUE, wellaboveNEG = TRUE, limIsGeneDetected = 50 and limNEG = 25.
