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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Analysis of gene expression change by gefitinib treatment in gefitinib sensitive PC9 and resistant PC9.

ABSTRACT: We established a gefitinib-resistant cell line (PC-9GR), by serial exposure of gefitinib to PC-9, an originally gefitinib-sensitive lung cancer cell line (PC-9na), for long period.We collected total RNA from both PC-9 and PC-9GR and examined mRNA expression profile, comprehensively. Gefitinib induced gene expression was measured in human lung cancer cell line was measured at 48 hours after exposure to 1uM Gefitinib.

ORGANISM(S): Homo sapiens

SUBMITTER: Junko Hamamoto

PROVIDER: E-GEOD-38302 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Analysis of gene expression change by gefitinib treatment in gefitinib sensitive PC9 and resistant PC9.

Project description:We established a gefitinib-resistant cell line (PC-9GR), by serial exposure of gefitinib to PC-9, an originally gefitinib-sensitive lung cancer cell line (PC-9na), for long period.We collected total RNA from both PC-9 and PC-9GR and examined mRNA expression profile, comprehensively.

2012-07-01 | GSE38302 | GEO

Time-course gene expression profiles of gefitinib-sensitive or -resistant lung adenocarcinoma cells stimulated with EGF, in the presence or absence of gefitinib, EGF receptor tyrosine kinase-specific inhibitor

Project description:Gefitinib, an epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), induces substantial clinical responses for non-small cell lung cancer (NSCLC) cells harboring EGFR activating mutations, but most of them invariably develop resistance. By generating a gefitinib resistance (PC9GR) from a human NSCLC-derived drug sensitive cell line (PC9), we studied differences of transcription dynamics between them by the aid of a computational decoupling of hidden regulatory signals from time course gene expression profiles. Given a collection of transcription factors (TFs) and their regulatory targets, the method captured temporally-synchronized shifts in evolving expression of target genes sharing each TF regulatory unit, and drew underlying regulatory signals. The analysis identified sterol regulatory element binding protein 1 (SREBP-1) as a key regulatory agent that facilitates the maintenance of drug tolerance, involving transcription controls of a G1-specific cyclin dependent kinase inhibitor whose expression was specifically elevated in PC9, but in turn, reduced in PC9GR Gefitinib-resistance cell line (PC9GR) was established derived from lung adenocarcinoma cell line PC9. PC9 cells and PC9GR cells were treated with the four different conditions, control (No treatment), EGF-treatment, gefitinib-treatment, and both gefitinib and EGF-treatment. In each condition, the gene expression was measured at 26 time points during 24 hrs.

2014-01-01 | E-GEOD-34228 | biostudies-arrayexpress

Transcriptome analysis of PC9 cells with gefitinib or/and hypoxia treatment and comparison with gefitinib resistant PC9 cells and ALDH positive PC9 cells

Project description:Inevitable gefitinib resistance and relapse of the disease was the biggest hurdle to NSCLC treatment. Importantly, the role of hypoxia in solid tumor tissues in vivo in gefitinib acquired resistance and its relationship to lung cancer stem cells (LCSCs) has not been fully elucidated. Here, the PC9 cells were treated with short term gefitinib or/and hypoxia, also, PC9 gefitnib resistant (PC9-GR) cell line was established and ALDH positive PC9 cells were sorted by FACs. Transcriptome analysis among those PC9 cell groups revealed the important role of hypoxia in gefitinib acquired resistance and signaling transduction change, which may critical for NSCLC disease progression and recurrence.

2017-10-31 | GSE69599 | GEO

The lncRNAs, circRNAs and mRNAs involved in gefitinib-resistance of PC9 cells

Project description:In this study, we established an gefitinib resistant lung adenocarcinoma cell line (i.e. PC9/GR) from lung adenocarcinoma PC9 cell line which was sensitive to gefitinib. Then microarray was performed to elucidate the lncRNAs, cirRNAs and mRNAs involved in gefitinib resistance.

2022-04-11 | GSE169513 | GEO

Integrative analysis of proteome and ubiquitylome reveals unique features of protein ubiquitylation and mitochondria in gefitinib resistant non-small cell lung cancer cells

Project description:Even though gefitinib, a tyrosine kinase inhibitor, widely used in treating non-small cell lung cancer (NSCLC) patients carrying EGFR activating mutations, most patients will develop gefitinib resistance. Protein ubiquitylation is one of major posttranslational modifications affecting the stability or function of the protein. However, the role of protein ubiquitylation in gefitinib resistance is poorly understood. To systematically identify the global change in protein ubiquitylation during gefitinib resistance, we carried out quantitative global proteome and ubiquitylome study by using cells with stable isotopic labeling with amino acid in cell culture (SILAC) followed by affinity enrichment of ubiquitylated peptides and subsequent liquid chromatography–tandem mass spectrometry (LC-MS/MS) analysis. Our study quantified are differentially regulated in ubiquitylation between gefitinib resistant and sensitive cells. Among them, 799 lysine sites were up-regulated in ubiquitylation in resistant cells, which are enriched in pathways, such as SNARE interaction in vesicle transport, endocytosis, phagosome, and lysosome, etc. In addition, we also found cells. The proteins carry these sites are involved in pathways including metabolic pathways, gap junction, and biosynthesis of amino acids, etc, This data indicate that gefitinib resistance dramatically alters the landscape of ubiquitylation in the cells. Furthermore, by integrating the genome-wide transcriptome data, we discovered that complexes I and IV in the electron transport chain of the mitochondria are up-regulated, while complexes II and III are down-regulated in resistant cells. Overall, these results reveal the unique features of ubiquitylation and mitochondria during gefitinib resistance, which will help to a better understanding of the role(s) of ubiquitylation, and to identify new therapeutic targets in overcoming gefitinib resistance.

2018-07-05 | PXD004941 | Pride

Genome-wide analysis of gefitinib short-term resistance gene expression in the NSCLC cell line PC9 in co-culture

Project description:Analysis of gefitinib short-term resistance at gene expression level. The hyposthesis tested in the present study was that short-term resistance towards gefitinib in NSCLC cells influences pathways that associates with resistance towards EGFR-TKI treatment. Results provide important information of the response of EGFR mutant NSCLC cells to gefitinib and also to resistance towards gefitinib resistance, up-or down-regulated specific resistance pathways and cellular functions. Total RNA obtained from PC9 cell line (n=3), co-cultured PC9 (with MRC-5 cells)(n=3), gefitinib treated (0.5ÂµM) PC9 (n=3), and co-cultured (MRC-5) + gefitinib treated PC9 cells (n=3) for 48h after gefitinib treatment

2016-07-01 | E-GEOD-75308 | biostudies-arrayexpress

IL-8 Confers Acquired Resistance to EGFR Inhibitors through Regulating Stem Cell-like Properties in Lung Cancer

Project description:Previous study has demonstrated that PC9/gef cells are resistant to gefitinib-induced aspoptosis. To investigate the regulators contributed to gefitinib resistance in lung cancer, we analyzed the gene expression profiles between PC9 and PC9/gef cells. Our results showed that IL-8 contributes to gefitinib resistance and cancer stemness. In contrast, IL-8 knockdown decreased stem-like characteristics and increased gefitinib-induced apoptosis in PC9/gef cells. RNAs extracted from gefitinib-sensitive PC9 cells and gefitinib-resistant PC9/gef cells were hybridized on Affymetrix microarrays. We tried to compare the differential gene expression profiles between PC9 and PC9/gef cells to identify the possible regulators in gefitinib resistance.

2015-08-12 | E-GEOD-60189 | biostudies-arrayexpress

Gene expression profiles of naïve PC-9 cells and PC-9GR cells that are resistant to gefitinib.

Project description:We investigated gene expression profiles of gefitinib-resistant PC-9 (PC-9GR) cells as well as naïve PC-9 cells. The data exhibited marked differences in the expression profiles between them.

2016-12-31 | GSE72197 | GEO

miRNA array analysis following gefinitib/luteolin administration to PC-3 cells

Project description:To determine if any altered miRNA expression is actually involved in the growth inhibition and/or cell death induction by luteolin and/or gefitinib, we performed miR-array analysis using RNA from PC-3 cells after 24h of treatment with 60Î¼M luteolin and/or 60Î¼M gefitinib. PC-3 cells were treated for 24h with DMSO, 60Î¼M luteolin (Lut), 60Î¼M gefitinib (Gef) or their co-administration (Lut+Gef). Each sample was run in duplicate.

2014-06-29 | E-GEOD-53178 | biostudies-arrayexpress

Genome-wide analysis of gefitinib short-term resistance gene expression in the NSCLC cell line PC9 in co-culture

2016-07-01 | GSE75308 | GEO

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