Effect of NORAD shRNA on A549 cells treated with TGF-beta
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE109296 | GEO | 2018/04/26
REPOSITORIES: GEO
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Project description:Effect of NORAD shRNA on A549 cells treated with TGF-beta
| PRJNA430367 | ENA
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.
2014-08-04 | GSE46024 | GEO
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. A549 cells were treated with or without 1ng/ml TGF-β for 12h. RNA was extracted and hybridized on Affymetrix microarrays
2014-08-04 | E-GEOD-46024 | biostudies-arrayexpress
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.
2009-09-15 | E-GEOD-17708 | biostudies-arrayexpress
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.
2009-08-20 | GSE17708 | GEO
Project description:Although numerous long noncoding RNAs (lncRNAs) have been identified, our understanding of their roles in mammalian physiology remains limited. Here we investigated the physiologic function of the conserved lncRNA Norad in vivo. Deletion of Norad in mice results in genomic instability and mitochondrial dysfunction, leading to a dramatic multi-system degenerative phenotype resembling premature aging. Loss of tissue homeostasis in Norad-deficient animals is attributable to augmented activity of PUMILIO proteins, which act as post-transcriptional repressors of target mRNAs to which they bind. Norad is the preferred RNA target of PUMILIO2 (PUM2) in mouse tissues and, upon loss of Norad, PUM2 hyperactively represses key genes required for mitosis and mitochondrial function. Accordingly, enforced Pum2 expression fully phenocopies Norad deletion, resulting in rapid-onset aging-associated phenotypes. These findings provide new insights and open new lines of investigation into the roles of noncoding RNAs and RNA binding proteins in normal physiology and aging.
2019-02-05 | GSE121688 | GEO
Project description:Gene expression profile of A549 cells treated with TGF-beta
| PRJNA563653 | ENA
Project description:Although numerous long noncoding RNAs (lncRNAs) have been identified, our understanding of their roles in mammalian physiology remains limited. Here we investigated the physiologic function of the conserved lncRNA Norad in vivo. Deletion of Norad in mice results in genomic instability and mitochondrial dysfunction, leading to a dramatic multi-system degenerative phenotype resembling premature aging. Loss of tissue homeostasis in Norad-deficient animals is attributable to augmented activity of PUMILIO proteins, which act as post-transcriptional repressors of target mRNAs to which they bind. Norad is the preferred RNA target of PUMILIO2 (PUM2) in mouse tissues and, upon loss of Norad, PUM2 hyperactively represses key genes required for mitosis and mitochondrial function. Accordingly, enforced Pum2 expression fully phenocopies Norad deletion, resulting in rapid-onset aging-associated phenotypes. These findings provide new insights and open new lines of investigation into the roles of noncoding RNAs and RNA binding proteins in normal physiology and aging.
2019-02-05 | GSE121684 | GEO
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.
2021-06-17 | GSE136780 | GEO
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.
2014-07-27 | E-GEOD-56356 | biostudies-arrayexpress