Homo sapiens
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-49644
PROVIDER: PRJNA214591 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcription profiling by array of three non-small cell lung cancer cell lines upon TGFb-induced epithelial-mesenchymal transition (EMT) against untreated counterparts to study EMT's role in tumour metastasis
2025-01-24 | E-GEOD-49644 | ExpressionAtlas
Project description:RNA-seq of TGF-beta induced and histone variant H2A.Z-knocked-down canine MDCK cells in epithelial-to-mesenchymal transition (EMT)
2017-11-23 | E-MTAB-5628 | ExpressionAtlas
Project description:cDNA expression array of epithelial phenotype untreated MDCK cells; after 30 days of TGFb treatment, which induces a mesenchymal phenotype; TGF-b-treated cells that are treated with 5-AZA for 72 h; and 30 days after TGFb withdrawal Gene expression was analyzed in a genome-wide manner, to asses those changes occurring upon TGF-b-induced epithelial to mesenchymal transition (EMT), those that are stimulated by treatment with a demethylating agent, and which are restored after TGF-b withdrawal Two replicates for untreated and TGFb treated, and one sample for 5-AZA and TGFb withdrawal
2014-08-14 | E-GEOD-48525 | biostudies-arrayexpress
Project description:Epithelial/mesenchymal transition (EMT) is associated with loss of cell adhesion molecules, such as E-cadherin, and increased invasion, migration, and proliferation in epithelial cancers. In non-small cell lung cancer (NSCLC), EMT is associated with greater resistance to EGFR inhibitors. However, its potential to predict response to other targeted drugs or chemotherapy has not been well characterized. The goal of this study was to develop a robust, platform-independent EMT gene expression signature and to investigate the association of EMT and drug response in NSCLC. A 76-gene EMT signature was derived in 54 DNA-fingerprinted NSCLC cell lines and tested in an independent set of cell lines and in NSCLC patients from the BATTLE clinical trial. The signature classified cell lines as epithelial or mesenchymal independent of the microarray platform and correlated strongly with E-cadherin protein levels, as measured by reverse phase protein array. Higher protein expression of Rab25 (in epithelial lines) and Axl (in mesenchymal lines), two signature genes associated with in EMT in other cancer types, was also confirmed. Mesenchymal cell lines demonstrated significantly greater resistance to EGFR inhibition, independent of EGFR mutation status and were more resistant to drugs targeting the PI3K/Akt pathway. We observed no association between EMT and response to cytotoxic chemotherapies, including cisplatin, pemetrexed, and docetaxel monotherapy and/or doublets (p-values ?0.2). In NSCLC patients, the EMT signature predicted 8-week disease control in the erlotinib arm, but not in other treatment arms. In conclusion, we have developed a robust EMT signature that predicts resistance to EGFR inhibitors and PI3K/Akt pathway inhibitors. To develop gene expression signatures for in vitro drug response and other phenotypes. Profiling was done on 68 NSCLC cell lines and 2 HBEC-KT cell lines (normal lung cells immortalized with CDK4 and hTERT).
2012-10-25 | E-GEOD-32989 | biostudies-arrayexpress
Project description:Epithelial-mesenchymal transition has been implicated in tumor metastasis, cancer drug resistance and cancer stem cell features. In this study, we examined gene expression profiles of three non-small cell lung cancer cell lines, before and after experimentally induced EMT. We modeled epitheial-mesenchyml transition by culturing A549, HCC827 and NCI-H358 cells in the presence of TGFb for three weeks, and compared gene expression profiles of the paretnal cells and cells after EMT.
2014-11-19 | E-GEOD-49644 | biostudies-arrayexpress
Project description:cDNA expression array of epithelial phenotype untreated MDCK cells; after 30 days of TGFb treatment, which induces a mesenchymal phenotype; TGF-b-treated cells that are treated with 5-AZA for 72 h; and 30 days after TGFb withdrawal Gene expression was analyzed in a genome-wide manner, to asses those changes occurring upon TGF-b-induced epithelial to mesenchymal transition (EMT), those that are stimulated by treatment with a demethylating agent, and which are restored after TGF-b withdrawal
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Project description:miRNAs are known to be involved in PDAC tumourigenesis. However, not many have been investigated in the context of TGFb-induced EMT. To identify novel miRNAs involved in this response, we performed a miRNA profiling study in PANC-1 cells treated with TGFb and additional PDAC lines with epithelial or mesenchymal characteristics.
2018-04-18 | GSE88756 | GEO
Project description:Epithelial/mesenchymal transition (EMT) is associated with loss of cell adhesion molecules, such as E-cadherin, and increased invasion, migration, and proliferation in epithelial cancers. In non-small cell lung cancer (NSCLC), EMT is associated with greater resistance to EGFR inhibitors. However, its potential to predict response to other targeted drugs or chemotherapy has not been well characterized. The goal of this study was to develop a robust, platform-independent EMT gene expression signature and to investigate the association of EMT and drug response in NSCLC. A 76-gene EMT signature was derived in 54 DNA-fingerprinted NSCLC cell lines and tested in an independent set of cell lines and in NSCLC patients from the BATTLE clinical trial. The signature classified cell lines as epithelial or mesenchymal independent of the microarray platform and correlated strongly with E-cadherin protein levels, as measured by reverse phase protein array. Higher protein expression of Rab25 (in epithelial lines) and Axl (in mesenchymal lines), two signature genes associated with in EMT in other cancer types, was also confirmed. Mesenchymal cell lines demonstrated significantly greater resistance to EGFR inhibition, independent of EGFR mutation status and were more resistant to drugs targeting the PI3K/Akt pathway. We observed no association between EMT and response to cytotoxic chemotherapies, including cisplatin, pemetrexed, and docetaxel monotherapy and/or doublets (p-values ≥0.2). In NSCLC patients, the EMT signature predicted 8-week disease control in the erlotinib arm, but not in other treatment arms. In conclusion, we have developed a robust EMT signature that predicts resistance to EGFR inhibitors and PI3K/Akt pathway inhibitors. Gene expression profiles were measured in 131 core biopsies from patients with refractory non-small cell lung cancer in the Biomarker-integrated Approaches of Targeted Therapy for Lung Cancer Elimination (BATTLE) trial. We used the BATTLE dataset to test an EMT gene expression signature trained in cell lines and independant of the microarray platform.
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Project description:TWIST1-induced microRNA-424 drives an intermediate epithelial-to-mesenchymal transition that opposes metastasis
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Project description:transcription profiling by array mouse mammary epithelial cells treated with TGF-beta to induce epithelial-to-mesenchymal transition
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