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Genome wide H3k27ac modification changes in Wild Type PC9 cells and MED13L knocking-down PC9 cells [H3K27ac ChIP-seq]

ABSTRACT: Silencing of MED13L impairs Mediator-regulated chromatin H3K27ac modification in NSCLC. Here, we performed H3K27ac ChIP-seq to investigate impacts of miR-4497 or knocking-down MED13L on chromatin H3K27ac modification in NSCLC PC9 cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE147120 | GEO | 2020/08/19

REPOSITORIES: GEO

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Genome wide H3k27ac modification changes in Wild Type PC9 cells and MED13L knocking-down PC9 cells [H3K27ac ChIP-seq]

Project description:Genome wide H3k27ac modification changes in Wild Type PC9 cells and MED13L knocking-down PC9 cells [H3K27ac ChIP-seq]

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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

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

Genome-wide map of H3K4me3 in erlotinib-resistant PC9 cells.

Project description:The non-small cell lung carcinoma (NSCLC) PC9 cell line is an established preclinical model for tyrosine kinase inhibitors. Recent evidence suggests that the H3K4 demethylase KDM5A protein is required for emerging drug-resistant cell populations. To better understand the dependence of cell survival on H3K4me3 level, we treated the EGFR-mutant PC9 cells with erlotinib and performed ChIP-seq analysis using H3K4me3 antibodies. We were able to identify genomic regions that exhibit decreased H3K4me3 in drug-treated cells. The results of this study will help to address clinical usefulness of KDM5A-targeted strategies in overcoming drug resistance, particularly in NSCLC.

2020-12-19 | GSE148461 | GEO

Single cell RNA sequencing analysis of freshly resected PC9 cell line-derived tumor xenografts

Project description:The non-small cell lung carcinoma (NSCLC) PC9 cell line is an established preclinical model for tyrosine kinase inhibitors. Using PC9 cells, we generated EGFR-mutant lung cancer xenografts to study the differences in response between individual cells and cell populations. We performed treatment of PC9 xenograft tumors with the combination of osimertinib and crizotinib as well as single drugs, followed by Drop-seq. The addition of crizotinib was guided by our previous data in PC9 grown in cell culture that identified an erlotinib-resistant drug population sensitive to crizotinib. The results of the xenograft study show that combination treatment targets specific osimertinib-tolerant cell populations but leaves a subset of the population that is tolerant to the combo. Each cell subpopulation is characterized by specific molecular signatures. The results of our study help to address emerging drug resistance that limits clinical usefulness of targeted strategies, particularly in NSCLC.

2020-12-19 | GSE160244 | GEO

Single cell RNA-seq profiling of erlotinib-resistant PC9 cells

Project description:The non-small cell lung carcinoma (NSCLC) PC9 cell line is an established preclinical model for tyrosine kinase inhibitors. To be able to better understand the differences in response between individual cells, we performed treatment of PC9 cells grown in cell culture with erlotinib followed by Drop-seq. We were able to clearly distinguish cells that were treated with the drug for 11 days from untreated cells, and we discovered different cell populations within the treated cells, likely reflecting heterogeneity of drug resistant cells. We were able to identify specific biomarkers, as preferentially expressed genes, for each cell population. The results of our study will address preexisting and acquired drug resistance that limits clinical usefulness of targeted strategies, particularly in NSCLC.

2020-12-19 | GSE149214 | GEO

Gene expression profiling of erlotinib-resistant PC9 cells.

Project description:The non-small cell lung carcinoma (NSCLC) PC9 cell line is an established preclinical model for tyrosine kinase inhibitors. To better understand gene expression changes in cells that survived the inhibitor treatment, we treated the EGFR-mutant PC9 cells with erlotinib, isolated RNA, and performed RNA-seq analysis. We were able to identify genes that are differentially expressed in erlotinib-treated cells compared to untreated. The results of this study will be integrated with single cell RNA-seq to address the utility of bulk RNA versus single cell RNA strategies in identifying biomarkers of drug resistance.

2020-12-19 | GSE148465 | GEO

Profiling non-small cell lung carcinoma cell line PC9 treated with erlotinib

Project description:The non-small cell lung carcinoma (NSCLC) PC9 cell line is an established preclinical model for tyrosine kinase inhibitors. To be able to better understand the differences in response between individual cells, we performed treatment of PC9 cells grown in cell culture with erlotinib followed by Drop-seq. We were able to clearly distinguish cells that were treated with the drug for five different time points from untreated cells, and we discovered different cell populations within the treated cells, likely reflecting heterogeneity of drug resistant cells. We were able to identify specific biomarkers, as preferentially expressed genes, for each cell population. The results of our study will address preexisting and acquired drug resistance that limits clinical usefulness of targeted strategies, particularly in NSCLC.

2020-12-19 | GSE134839 | GEO

Profiling non-small cell lung carcinoma cell line PC9 treated with erlotinib using 10x Genomics

Project description:The non-small cell lung carcinoma (NSCLC) PC9 cell line is an established preclinical model for tyrosine kinase inhibitors. To be able to better understand the differences in response between individual cells, we performed treatment of PC9 cells grown in cell culture with erlotinib followed by 10x Genomics. We were able to clearly distinguish cells that were treated with the drug from untreated cells, and we discovered different cell populations within the treated cells, likely reflecting heterogeneity of drug resistant cells. We were able to identify specific biomarkers, as preferentially expressed genes, for each cell population. The results of our study will address preexisting and acquired drug resistance that limits clinical usefulness of targeted strategies, particularly in NSCLC.

2020-12-19 | GSE134836 | GEO

Comparison of gene expression in xenograft tissue stably expressing ShRNA KDM1A

Project description:The purpose of this study was to chacterise the effect of KDM1A knocking down on genome-wide gene expression in human NSCLC cells in vivo. Affymetrix human transcriptome array 2.0 was used to profile the transcriptome of xenograft tumors derived from PC9 cells stably expressing either ShRNA KDM1A or ShRNA control. These cells were subcutanously injected into the right axillary of the mouse, and allowd to grow for 5 weeks to form xenograft tumors. Although KDM1A is up-regulated in NSCLC, but key genes and pathways regulated by KDM1A was not well-understood in NSCLC. Using this approach, we have shown that KDM1A repressed or activated a distinctive set of pathways and key target genes in vivo. This first comprehesive study of transciptome profile upon KDM1A koncking-down in vivo highlights the distinctive pathways regulated by KDM1A during NSCLC tumorigenesis, and it will help to identify new therapeutic targets for NSCLC treatment. Xenograft tumors derived from two cell lines: PC9 cells stably expressing ShRNA KDM1A or ShRNA control. We extracted total RNA from 3 independent xenograft tumors per cell line.

2016-07-27 | E-GEOD-71358 | biostudies-arrayexpress

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