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FOXM1 variant contributes to gefitinib resistance via activating wnt/β-catenin signal pathway in non-small cell lung cancer patients

ABSTRACT: To further explore the functional role of rs3742076 in the regulation of gefitinib response, stable overexpression FOXM1 rs3742076_A and _G were established in PC9 cells in which FOXM1 knock-out by CRISPR/Cas9.

ORGANISM(S): Homo sapiens

PROVIDER: GSE201020 | GEO | 2022/05/25

REPOSITORIES: GEO

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FOXM1 variant contributes to gefitinib resistance via activating wnt/β-catenin signal pathway in non-small cell lung cancer patients

Project description:FOXM1 variant contributes to gefitinib resistance via activating wnt/β-catenin signal pathway in non-small cell lung cancer patients

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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

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

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

PIPseq on Gefitinib sensitive and resistant cell lines

Project description:We used PIP-seq single cell RNA-sequencing to study the response of PC9 and H1975 to Gefitinib

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Gefitinib treatment in human EGFR-driven-Gefitinib resistant tumoral cell line

Project description:In order to analyze the molecular effect of the combination of Notch inhibitors and EGFR inhibitors on resistance to TKI, we performed RNA-seq gene expression profiling of PC9 resistant to Gefitinib cells treated with different combinations.

2021-07-01 | GSE117846 | 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.

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Apatinib preferentially inhibits Gefitinib-resistant lung cancer cells by inducing cell cycle arrest and inhibiting VEGFR signaling pathway

Project description:Targeted therapy for patients with EGFR mutations by tyrosine kinase inhibitors (TKIs) has provided a significant benefit to patients. However, gradually developed resistance to the therapy becomes a major challenge in clinical practice. Herein, we report that Apatinib, an anti-angiogenic drug, strongly and specifically inhibits Gefitinib-resistant cancer cells but not their parental sensitive cells. Gefitinib-resistant lung cancer cell line (PC9GR) was established from its parental sensitive line (PC9) with a traditional EGFR mutation after long time exposure to Gefitinib. The established PC9GR cells had over 250 fold increased resistance to Gefitinib than its sensitive parental PC9 cells. Apatinib demonstrated much stronger (~5 fold) growth inhibition on PC9GR cells than on PC9 and other lung cancer cell lines. This inhibition was mostly achieved through cell cycle rest in G1 phase as demonstrated by transcriptome and protein expression data. Oral intake of Apatinib in mouse model significantly inhibited establishment and growth of PC9GR implanted tumors. VEGFR2 phosphorylation in PC9GR tumors after Apatinib treatment was significantly reduced along with less micro-vessel formation. Apatinib may provide a benefit to patients with acquired resistance to TKI treatment.

2019-05-15 | GSE129221 | GEO

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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RNA-seq of PC9 cells tolerant to gefitinib

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