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Profiling non-small cell lung carcinoma cell line PC9 treated with etoposide, erlotinib and its combination with crizotinib

ABSTRACT: Profiling non-small cell lung carcinoma cell line PC9 treated with etoposide, erlotinib and its combination with crizotinib

PROVIDER: PRJNA627675 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11597466_1.fastq.gz	Fastqsanger.gz
	SRR11597466_2.fastq.gz	Fastqsanger.gz
	SRR11597467_1.fastq.gz	Fastqsanger.gz
	SRR11597467_2.fastq.gz	Fastqsanger.gz
	SRR11597468_1.fastq.gz	Fastqsanger.gz

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Profiling non-small cell lung carcinoma cell line PC9 treated with etoposide, erlotinib and its combination with crizotinib

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 etoposide, erlotinib and its combination with crizotinib, followed by Drop-seq. The addition of crizotinib was guided by our previous data that an erlotinib-resistant drug population may be sensitive to crizotinib. To better understand the common events in drug resistance, we compared the resistant cell populations arising from the treatment with etoposide and from the treatment with erlotinib. The results of our study will address emerging drug resistance that limits clinical usefulness of conventional and targeted strategies, particularly in NSCLC.

2020-12-19 | GSE149215 | 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.

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gene expression profiles in PC9 erlotinib resistance cells after erlotinib, HDAC inhibitor YF454A or combination treatment

Project description:To identify the potential mechanisms of enhanced activity of combined inhibition of erlotinib and YF454A, we conducted a microarray analysis on gene expression profiles in PC9 erlotinib cells. We used Affymetrix GeneChip® Human Transcriptome Array 2.0 to detail gene expression after indicated treatments and identified the molecular mechanism during this process to facilitate further studies.

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RNA sequencing of PC9 and four erlotinib-persister cells derived from PC9

Project description:Given the recent reports on the role of AXL in mediating resistance to EGFR-targeted therapy, we generated cell line models of Erlotinib-resistance to investigate the effect of AXL inhibitors on EGFR TKI resistance. For this, EGFR-mutant PC9 cells were passed through a persister bottleneck by applying strong drug selection pressure to generate drug-tolerant erlotinib persister cells. We created four Erlotinib-resistant clones from one parental population; S1-34, S2-10, S2-17 and S2-30. Whole exome and RNA sequencing analyses were performed to probe the differences in Erlotinib-resistance mechanisms present in these persister-derived Erlotinib-resistant cells.

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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.

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Charaterization of genetic alterations and gene expression signatures found in erlotinib-resistant and erlotinib/crizotinib dual-resistant HCC827 subpopulations

Project description:The non-small cell lung cancer (NSCLC) cell line HCC827 harbors an activating EGFR mutation (exon 19 deletion) that confers sensitivity to the FDA-approved EGFR inhibitor erlotinib. By applying the ClonTracer barcoding system, we were able to show the presence of pre-existing sub-populations in HCC827 that contribute to erlotinib resistance. Prior studies implicated that MET amplification confers resistance to erlotinib in this cell line. Therefore we examined the effects of the c-Met inhibitor crizotinib on the barcoded HCC827 population when treated either sequentially or simultaneously with both inhibitors. Despite the significant reduction in barcode complexity, the erlotinib/crizotinib combination treatment failed to eradicate all of the resistant clones implying the presence of an erlotinib/crizotinib dual resistant subpopulation. We performed transcriptome profiling (RNA-seq) to elucidate the potential resistance mechanisms of the dual resistant subpopulation in comparison to vehicle-treated or single agent erlotinib-resistant HCC827 cell populations as controls. mRNA profiling of the subpopulations of human NSCLC cell line HCC827 that contribute to EGFR inhibitor erlotinib and MET inhibitor crizotinib resistance

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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.

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Charaterization of genetic alterations and gene expression signatures found in erlotinib-resistant and erlotinib/crizotinib dual-resistant HCC827 subpopulations

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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.

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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.

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