Homo sapiens
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-52143
PROVIDER: PRJNA227472 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Examination of genome-wide methylation changes in lung cancer cell lines A549 (A) and HTB56 (H) [HumanMethylation27 BeadChip experiments]
| PRJNA227470 | ENA
Project description:Cancer cell phenotypes are partially determined by epigenetic specifications such as DNA methylation. Metastasis development is a late event in cancerogenesis and might be associated with epigenetic alterations. Here, we analyzed genome wide DNA methylation changes that were associated with pro-metastatic phenotypes in non-small cell lung cancer using the Illumina HumanMethylation27 BeadChip platform. We studied genome-wide methylation changes in lung cancer cell lines A549 (A) and HTB56 (H). We generated NSCLC lines with highly increased propensity to form tumor nodules in murine lungs after intravenous injections. In addition to the normal cell lines (0R) we analyzed the methylome of the the cell lines after three rounds of in vivo selection towards a highly metastatic phenotype (3R).
2013-12-18 | E-GEOD-52144 | biostudies-arrayexpress
Project description:Genome-wide DNA-methylation profiles of human lung cancer cell lines and normal lung cells were generated by Infinium bead chip technology DNA methylation patterns of over 480,000 CpG sites were analyzed in normal human bronchial epithelial cells (NHBEC) and three non small cell lung cancer cell lines (NSCLC: A427, A549 and H322) using bisulfite-based Illumina 450K BeadChip arrays
2017-08-15 | GSE92843 | GEO
Project description:Cancer cell phenotypes are partially determined by epigenetic specifications such as DNA methylation. Metastasis development is a late event in cancerogenesis and might be associated with epigenetic alterations. Here, we analyzed genome wide DNA methylation changes that were associated with pro-metastatic phenotypes in non-small cell lung cancer with Reduced Representation Bisulfite Sequencing. DNMT-inhibition by 5-Azacytidine at low concentrations reverted the pro-metastatic phenotype. 5-Azacytidine led to preferential loss of DNA methylation at sites that were DNA hypermethylated during the in vivo selection. Changes in DNA methylation persisted over time. Keywords: Methylation profiling by high throughput sequencing We studied genome-wide methylation changes in lung cancer cell lines A549 (A) and HTB56 (H). We generated NSCLC lines with highly increased propensity to form tumor nodules in murine lungs after intravenous injections. In addition to the normal cell lines (0R) we analyzed the methylome of the the cell lines after three rounds of in vivo selection towards a highly metastatic phenotype (3R). Next we studied changes in the methylome of highly metastatic cell lines after DNA Methyltransferase inhibition by 5-Azacytidine treatment at low concentrations (250 nM & 1000 nM) for 6 days. During treatment cells were supplemented with fresh medium every 48 hours. After 6 days of 5-Azacytidine exposure, cells were washed three times with PBS to wash out the drug. The cells were released for additional 7 days in regular medium. We followed up the DNA methylation changes at day 13 of the experiment.
2013-12-18 | E-GEOD-52140 | biostudies-arrayexpress
Project description:To determine the signaling networks that are dysregulated in cisplatin-resistant non-small cell lung cancer, noncoding RNA expression data were obtained from, and compared between, the lung adenocarcinoma cell line, A549, and its cisplatin-resistant derivative, A549/CDDP. Noncoding RNA expression data from a cisplatin-sensitive lung adenocarcinoma cancer cell line (A549) were collected and compared to noncoding RNA expression data from a cisplatin-resistant cell line (A549/CDDP). 3 independent experiments were completed for both the sensitive and resistant cell lines.
2013-01-15 | E-GEOD-43249 | biostudies-arrayexpress
Project description:To determine the signaling networks that are dysregulated in cisplatin-resistant non-small cell lung cancer, noncoding RNA expression data were obtained from, and compared between, the lung adenocarcinoma cell line, A549, and its cisplatin-resistant derivative, A549/CDDP. Noncoding RNA expression data from a cisplatin-sensitive lung adenocarcinoma cancer cell line (A549) were collected and compared to noncoding RNA expression data from a cisplatin-resistant cell line (A549/CDDP). 3 independent experiments were completed for both the sensitive and resistant cell lines.
2013-01-15 | E-GEOD-43493 | biostudies-arrayexpress
Project description:The goal of this study is to identify those genes that are commonly silenced by DNA-methylation in lung cancer cell lines. Experiment Overall Design: Ten lung cancer cell lines (Calu 1, Hotz, U1752, Calu 6, ZL25, Calu3, SW2, A549, H125, and H 460) were analyzed before and after the treatment with 5-aza-2âdeoxycitidine and trychostatin A (5AzaC/TSA).
2009-08-09 | E-GEOD-14315 | biostudies-arrayexpress
Project description:DNA methylation is tightly linked with gene expression regulation and has long been regarded a stable epigenetic mark in postmitotic cells. However, it recently became clear that postnatal brains appear to show stimulus-induced de novo CpG methylation or active demethylation related to neuronal plasticity. Due to striking homologies between the brains of birds and mammals, songbirds, especially the zebra finch, propose an attractive model for investigating the genome-wide DNA methylation profile and DNA methylation reconfiguration during brain development. In order to obtain a first genome-wide compendium of genes under putative DNA methylation control, we performed MethyCap-seq experiments on two recently cultured zebra finch cell lines, G266 and ZFTMA, also upon AZA-induced demethylation. First, the MethylCap-seq methodology in zebra finch was validated by comparison with RRBS generated data. Subsequently, quantitative analysis identified 30,700 significantly demethylated loci upon AZA-treatment. Further examination revealed enrichment of these regions in exons and promoters. To assess the influence of methylation on gene expression, RNA-seq experiments were performed. Comparison of the RNA-seq and MethylCap-seq results showed that at least 357 of the 3,457 AZA-upregulated genes are putatively regulated by methylation in the promoter region, for which a pathway analysis showed obvious enrichment for neurological networks. A subset of genes was validated using qPCR and CpG pyrosequencing. To our knowledge, this study provides the first genome-wide DNA methylation map of the zebra finch genome as well as a comprehensive set of genes of which transcription is under putative methylation control. MethylCap-seq and RNA-seq experiments were performed on DMSO- and AZA-treated zebra finch cell lines, i.e. G266 and ZFTMA. As a quality control, also an untreated ZFTMA sample was analyzed with MethylCap-seq and RRBS.
2015-12-10 | E-GEOD-61060 | biostudies-arrayexpress
Project description:GPX3 has been reported to be involved in antioxidant, anticancer, and anti-inflammation in various studies. It is also known that expression of GPX3 is low in lung cancer tissues. We performed a microarray using three lung cancer cell lines including A549, H1650, and H1975 lung cancer cell lines. Among these, A549 is highly expressed in GPX3 as compared with H1650 and h1975. Microarrays were used to analyze microRNAs showing other expression between A549 and the other two cell lines.
2019-01-23 | GSE125018 | GEO
Project description:Non-small cell lung cancer (NSCLC) is the most lethal and prevalent type of lung cancer. In almost all types of cancer, the levels of polyamines (putrescine, spermidine, and spermine) are increased, playing a pivotal role in tumor proliferation. Indomethacin, a non-steroidal anti-inflammatory drug, increases the abundance of an enzyme termed spermidine/spermine-N1-acetyltransferase (SSAT) encoded by the SAT1 gene. This enzyme is a key player in the export of polyamines from the cell. The aim of this study was to compare the effect of indomethacin on two NSCLC cell lines, and their combinatory potential with polyamine-inhibitor drugs in NSCLC cell lines. A549 and H1299 NSCLC cells were exposed to indomethacin and evaluations included SAT1 expression, SSAT levels, and the metabolic status of cells. Moreover, the difference in polyamine synthesis enzymes among these cell lines as well as the synergistic effect of indomethacin and chemical inhibitors of the polyamine pathway enzymes on cell viability were investigated. Indomethacin increased the expression of SAT1 and levels of SSAT in both cell lines. In A549 cells, it significantly reduced the levels of putrescine and spermidine. However, in H1299 cells, the impact of treatment on the polyamine pathway was insignificant. Also, the metabolic features upstream of the polyamine pathway (i.e., ornithine and methionine) were increased. In A549 cells, the increase of ornithine correlated with the increase of several metabolites involved in the urea cycle. Evaluation of the levels of the polyamine synthesis enzymes showed that ornithine decarboxylase is increased in A549 cells, whereas S-adenosylmethionine-decarboxylase and polyamine oxidase are increased in H1299 cells. This observation correlated with relative resistance to polyamine synthesis inhibitors eflornithine and SAM486 (inhibitors of ornithine decarboxylase and S-adenosyl-L-methionine decarboxylase, respectively), and MDL72527 (inhibitor of polyamine oxidase and spermine oxidase). Finally, indomethacin demonstrated a synergistic effect with MDL72527 in A549 cells and SAM486 in H1299 cells. Collectively, these results indicate that indomethacin alters polyamine metabolism in NSCLC cells and enhances the effect of polyamine synthesis inhibitors, such as MDL72527 or SAM486. However, this effect varies depending on the basal metabolic fingerprint of each type of cancer cell.
2021-02-08 | MTBLS873 | MetaboLights