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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Daisuke Okuzaki

PROVIDER: E-GEOD-53178 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gefitinib and luteolin cause growth arrest of human prostate cancer PC-3 cells via inhibition of cyclin G-associated kinase and induction of miR-630.

Sakurai Minami A MA Ozaki Yuki Y Okuzaki Daisuke D Naito Yoko Y Sasakura Towa T Okamoto Ayumi A Tabara Hiroe H Inoue Takao T Hagiyama Man M Ito Akihiko A Yabuta Norikazu N Nojima Hiroshi H

PloS one 20140627 6

Cyclin G-associated kinase (GAK), a key player in clathrin-mediated membrane trafficking, is overexpressed in various cancer cells. Here, we report that GAK expression is positively correlated with the Gleason score in surgical specimens from prostate cancer patients. Embryonic fibroblasts from knockout mice expressing a kinase-dead (KD) form of GAK showed constitutive hyper-phosphorylation of the epidermal growth factor receptor (EGFR). In addition to the well-known EGFR inhibitors gefitinib an ...[more]

PMID: 24971999

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Microarray analysis following gefinitib/luteolin administration to PC-3 cells

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-06-30 | E-GEOD-53181 | 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.

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Project description:To probe into the potential mechanisms contributing to the strong synergistic interaction between gefitinib and pemetrexed, gene expression profiles of PC-9 cells exposed to gefitinib, pemetrexed or combined treatment were analyzed using microarray technique.

2020-03-12 | E-MTAB-8661 | biostudies-arrayexpress

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. Gefitinib induced gene expression was measured in human lung cancer cell line was measured at 48 hours after exposure to 1uM Gefitinib.

2012-06-30 | E-GEOD-38302 | biostudies-arrayexpress

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 60μM luteolin and/or 60μM gefitinib.

2014-06-29 | GSE53178 | GEO

Inhibition of p300 Lysine Acetyltransferase activity by Luteolin reduces tumor growth in head and neck squamous cell carcinoma (HNSCC) xenograft mouse model [mRNA]

Project description:Chromatin acetylation is attributed with distinct functional relevance with respect to gene expression in normal and diseased conditions thereby leading to a topical interest in the concept of epigenetic modulators and therapy. We report here the identification and characterization of the acetylation inhibitory potential of an important dietary flavonoid, luteolin. Luteolin was found to inhibit p300 acetyltransferase with competitive binding to the acetyl CoA binding site. Luteolin treatment in a xenografted tumor model of head and neck squamous cell carcinoma (HNSCC), led to a dramatic reduction in tumor growth within 4 weeks corresponding to a decrease in histone acetylation. Cells treated with luteolin exhibit cell cycle arrest and decreased cell migration. Luteolin treatment led to an alteration in gene expression and miRNA profile including up-regulation of p53 induced miR-195/215, let7C; potentially translating into a tumor suppressor function. It also led to down-regulation of oncomiRNAs such as miR-135a, thereby reflecting global changes in the microRNA network. Furthermore, a direct correlation between the inhibition of histone acetylation and gene expression was established using chromatin immunoprecipitation on promoters of differentially expressed genes. A network of dysregulated genes and miRNAs was mapped along with the gene ontology categories, and the effects of luteolin were observed to be potentially at multiple levels: at the level of gene expression, miRNA expression and miRNA processing. Cells treated with luteolin exhibit cell cycle arrest and decreased cell migration. Luteolin treatment led to an alteration in gene expression and mRNA profile

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DNA microarray analysis following gefinitib/luteolin administration to PC-3 cells

Project description:To further investigate the molecular mechanism of cell death induction by luteolin and/or gefitinib, we performed DNA microarray analysis, which may reveal the change of gene expression pattern following treatment with these chemicals. We examined PC-3 cells after 24h of treatment with 60μM luteolin and/or 60μM gefitinib because subG1 population has not appeared yet at this timing, which helps to avoid the secondary effects of apoptosis on the alteration of the gene expression pattern.

2014-06-29 | GSE53180 | GEO

Transcription profiling of mouse microglia reveals luteolin has anti-inflammatory and neurotrophic effects on microglia

Project description:Our aim was to identify genes that were differentially expressed in microglia stimulated with Lipopolysaccharide, Luteolin, or both. Affymetrix microarrays were used to analyze RNA samples Experiment Overall Design: RNA from control BV-2 cells, and cells treated for 24h with LPS, Luteolin, or LPS+Luteolin was analyzed with Affymetrix GeneChip Mouse Genome 430 2.0 Arrays. Biological triplicates were analyzed for each condition

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

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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

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