Project description:We have previously demonstrated that TNF-α, a proinflammatory cytokine, enhances TGF-β-mediated EMT in A549 human lung cancer cells. RNA-sequencing analysis on CMT64 cells following TGF-β and/or TNF-α treatment revealed a subset of genes possibly regulated by TGF-β and/or TNF-α.
Project description:Time Course of TGF-beta treatment of A549 lung adenocarcinoma cell line on Affymetrix HG_U133_plus_2 arrays; triplicate experiments. The goal of the experiment is to profile temporal gene expression changes during TGF-beta-induced epithelial-mesenchymal transition (EMT). During EMT cancer cells loose their epithelial specifc proteins and gain mesenchymal proteins to acquire migratory and invasive phenotype essential for metastasis. Human A549 lung adenocarcinoma cell line was treated with 5 ng/mL TGF-beta for 0, 0.5, 1, 2, 4, 8, 16, 24, and 72 h to induce EMT. The experiment was repeated 3 times. Samples were assayed using Affymetrix HG_U133_plus_2 arrays with 54675 probe-sets, using standard techniques. We provide the raw .CEL files and a supplementary Excel spreadsheet with log-transformed data and selected results from a statistical analysis. Experiment Overall Design: Human A549 lung adenocarcinoma cell line was treated with 5 ng/mL TGF-beta for 0, 0.5, 1, 2, 4, 8, 16, 24, and 72 h. The experiment was repeated 3 times. Samples were assayed using Affymetrix HG_U133_plus_2 arrays with 54675 probe-sets, using standard techniques. The 2 h sample of the third experiment was not run on an array due to poor RNA, so that only 26 arrays were run.
Project description:We evaluated the effect of NORAD (also known as LINC00657 or LOC647979) shRNA on TGF-beta induced changes in the gene expression in A549 cells by RNA-seq.
Project description:Time Course of TGF-beta treatment of A549 lung adenocarcinoma cell line on Affymetrix HG_U133_plus_2 arrays; triplicate experiments. The goal of the experiment is to profile temporal gene expression changes during TGF-beta-induced epithelial-mesenchymal transition (EMT). During EMT cancer cells loose their epithelial specifc proteins and gain mesenchymal proteins to acquire migratory and invasive phenotype essential for metastasis. Human A549 lung adenocarcinoma cell line was treated with 5 ng/mL TGF-beta for 0, 0.5, 1, 2, 4, 8, 16, 24, and 72 h to induce EMT. The experiment was repeated 3 times. Samples were assayed using Affymetrix HG_U133_plus_2 arrays with 54675 probe-sets, using standard techniques. We provide the raw .CEL files and a supplementary Excel spreadsheet with log-transformed data and selected results from a statistical analysis.
Project description:To find out genes regulated by TGF-β in A549 cells, we compared gene expression of cells treated with 1ng/ml TGF-β versus non-treated cells and find out that expression of one transmembrane protein, TM4SF20, is reduced by TGF-β.
Project description:Control, 0.5 mM extracellular ATP and 10 ng/ml TGF-beta were used to treated 5 million A549 lung cancer cells in vitro for 2, 6 and 12 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 extracellular ATP and TGF-beta (a known EMT inducer).
Project description:TTF-1/NKX2-1 was expressed by adenoviral vector and changes in gene expression were determined by RNA-sequencing. A549 cells were infected with Ad-TTF-1 or Ad-LacZ vectors and stimulated with TGF-beta for 24 hours or left untreated. Expression of polyA RNA was determined.
Project description:Epithelial–mesenchymal transition (EMT) is a plastic process that converts epithelial cells into migratory and invasive cells. Accumulating evidence indicates that EMT is a key event for metastasis in several types of cancer, including non-small cell lung cancer (NSCLC). Especially, transforming growth factor-beta (TGF-beta) acts as a potent inducer of EMT and contributes to cancer progression. Emerging studies suggest that a metabolic reprograming is essential to acquire the EMT phenotype in cancer cells. However, a comprehensive understanding of metabolism in cancer EMT remains largely unexplored. Here, we analyzed metabolic changes during TGF-beta-induced EMT in NSCLC A549 cells using capillary electrophoresis time-of-flight mass spectrometry (CE-TOFMS). At the same time, we examined the expression of metabolic-related genes using microarray analysis.
