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MRNA expression profile of A549 cells and MSR-A549 cells with or without JQ1 treatment

ABSTRACT: To establish effective multitargeted KRAS pathway therapy, we analyzed mediators of acquired resistance to chronic momelotinib and MEK inhibitor exposure in A549 cells. Since inhibitor resistance was completely reversible after drug withdrawal for several passages, suggesting epigenetic reprogramming, we investigated whole mRNA expression profiles in A549, momelotinib and selumetinib resistant (MSR)-A549 cells and MSR-A549 cells following drug withdrawal for 10 days. In parallel, we also examined mRNA expression profiles of MSR-A549 cells treated with the BET inhibitor JQ1, to identify specific targets regulated by H3K27 acetylation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE96779 | GEO | 2019/03/28

REPOSITORIES: GEO

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Genome-wide maps of histone H3K27 acetylation in A549 and MSR-A549 cells.

Project description:To establish effective multitargeted KRAS pathway therapy, we analyzed mediators of acquired resistance to chronic momelotinib and MEK inhibitor exposure in A549 cells. Since inhibitor resistance was completely reversible after drug withdrawal for several passages, suggesting epigenetic reprogramming, we examined genome-wide H3K27 histone acetylation in parental A549 and momelotinib and selumetinib resistant (MSR)-A549 cells.

2019-03-28 | GSE96780 | GEO

A549 cells and MSR-A549 cells

Project description:A549 cells and MSR-A549 cells

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Withdrawal of MEK1/2 inhibitor reverses acquired resistance driven by BRAF amplification but drives EMT and chemoresistance in cells with amplified KRAS

Project description:Acquired resistance to MEK1/2 inhibitors can arise through amplification of BRAFV600E or KRASG13D to reinstate ERK1/2 signalling. Here we show that BRAFV600E amplification and selumetinib resistance are fully reversible following drug withdrawal. Resistant cells with BRAFV600E amplification become addicted to selumetinib to maintain a precise level of ERK1/2 signalling (2-3% of total ERK1/2 active, here quantified by mass spectrometry), that is optimal for cell survival and proliferation. The magnitude of ERK1/2 activation following selumetinib withdrawal (~20% active) drives a p57KIP2-dependent G1 cell cycle arrest and senescence or expression of NOXA and cell death, which selects against those cells with amplified BRAFV600E. ERK1/2-dependent p57KIP2 expression is required for loss of BRAFV600E amplification and determines the rate of reversal of selumetinib resistance. Furthermore, growth of selumetinib-resistant cells with BRAFV600E amplification as tumour xenografts is inhibited in mice that do not receive selumetinib. Thus, BRAFV600E amplification confers a selective disadvantage during drug withdrawal, providing a rationale for intermittent dosing to forestall resistance. In striking contrast, selumetinib resistance driven by KRASG13D amplification is not reversible. In these cells ERK1/2 reactivation does not inhibit proliferation but drives a ZEB1-dependent epithelial-to-mesenchymal transition that increases cell motility and promotes resistance to traditional chemotherapy agents arguing strongly against the use of ‘drug holidays’ in cases of KRASG13D amplification.

2019-03-11 | GSE120993 | GEO

RNA-seq profiling of A549 cells with sgRNA knockouts that confer prexasertib resistance

Project description:A549 cells with FOXM1 or LIN54 sgRNA knockout, which confers resistance to the CHK1 inhibitor prexasertib, were generated. These cells and control (empty vector) cells were synchronized in S phase, released for 1 hour and treated with 100 nM prexasertib or DMSO (vehicle) for 2 hours. RNA-seq profiling was performed to identify drug-induced perturbations in gene expression in these cells.

2021-02-24 | GSE154545 | GEO

A549 vs. A549DDP miRNA and mRNA analysis using RNA-seq

Project description:This study aims to identify pathway involvement in the development of cisplatin (cis-diamminedichloroplatinum (II); CDDP) resistance in A549 lung cancer (LC) cells by utilizing advanced bioinformatics software. We developed CDDP-resistant A549 (A549/DDP) cells through prolonged incubation with the drug and performed RNA-seq on RNA extracts to determined differential mRNA and miRNA expression between A549/DDP and A549 cells

2021-05-31 | GSE157692 | GEO

Gene copy number variation profiling by microarray

Project description:Here, we investigate focal amplification patterns in and around the BRAF locus in BRAFV600Emutant COLO205 cells that acquire resistance to the MEK inhibitor Sleumetinib / AZD6244 / ARRY-142886. We find that BRAF amplifications occur frequently in COLO205 cells during acquisition of selumetinib resistance and that BRAFamplifications pre-exist selumetinib treatment but occurs predominantly via de novo mutations

2021-03-23 | GSE168603 | GEO

Whole-transcriptome sequencing of A549 cells and cisplatin-resistance A549/DPP cells

Project description:Whole-transcriptome sequencing of A549 cells and cisplatin-resistance A549/DPP cells

| PRJNA603901 | ENA

miRNA expression of lung cancer cells A549 and cisplatin (DDP) resistant lung cancer cells A549/DDP

Project description:To investigate the difference of miRNA expression between lung cancer cell A549 and its DDP-resistant cell strain A549/DDP, we have employed miRNA microarray expression to discover the difference expression of miRNAs of A549 cells and A549/DDP. We conducted RT-qPCR to examine the expression levels of top differential expressed miRNAs, namely, miR-197-5p, miR-4443, miR-642a-3p, miR-27b-3p and miR-100-5p, confirming low variability between two methods. The A549/DDP was established from A549 in our laboratory, by exposing A549 to gradually increasing DDP concentrations, until the final concentration at 1Î¼g/ml. To avoid the influence of drug to the A549/DDP cells, they were cultured in a drug-free medium for at least two weeks before gene expression analysis. miRNA expression of A549 and A549/DDP was then analzyed.

2016-08-16 | E-GEOD-85603 | biostudies-arrayexpress

miRNA expression of exosomes derived from lung cancer cells A549 and cisplatin (DDP) resistant lung cancer cells A549/DDP

Project description:To investigate the difference of miRNA expression in exosomes derived from A549 cells and its DDP-resistant cell strain A549/DDP, we have employed miRNA microarray expression to discover the difference expression of miRNAs in exosomes derived from A549 and A549/DDP. We conducted RT-qPCR to examine the expression levels of top differential expressed miRNAs, namely, miR-197-5p, miR-4443, miR-642a-3p, miR-27b-3p and miR-100-5p, confirming low variability between two methods. The A549/DDP was established from A549 in our laboratory, by exposing A549 to gradually increasing DDP concentrations, until the final concentration at 1Î¼g/ml. To avoid the influence of drug to the A549/DDP cells, they were cultured in a drug-free medium for at least two weeks before gene expression analysis. After being incubated for 48-72h, the culture medium of cells was harvested. Exosomes were isolated by ultracentrifugation. And miRNA expression of exosomes derived from A549 and A549/DDP was then analzyed.

2016-08-16 | E-GEOD-85604 | biostudies-arrayexpress

A549 Sagopilone

Project description:Anticancer drug sagopilone in lung cancer line A549. We performed gene expression analysis of lung cancer cell line A549 treated with sagopilone and paclitaxel. The aim was to analyse gene expression differences between the two drugs in two different concentrations. A549 cells were treated with medium containing either 2.5 nM sagopilone, 40 nM sagopilone, 4 nM paclitaxel or 40 nM paclitaxel, respectively, vehicle (ethanol 0.1%), or were left untreated for 18 hours. The two different concentrations were chosen according the phenotypes they have caused in A549 cells. Treatment with 2.5 nM sagopilone, 4 nM paclitaxel induced an aneuploid cell population, whereas treatment with 40 nM sagopilone and 40 nM paclitaxel induced mitotic arrest.

2012-01-01 | E-MTAB-377 | biostudies-arrayexpress

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