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Genome-scale CRISPR screening identifies cell cycle and protein ubiquitination processes as druggable targets for erlotinib-resistant lung cancer

ABSTRACT: Genome-scale CRISPR screening identifies cell cycle and protein ubiquitination processes as druggable targets for erlotinib-resistant lung cancer

PROVIDER: PRJNA597891 | ENA |

REPOSITORIES: ENA

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Genome-scale CRISPR screening identifies cell cycle and protein ubiquitination processes as druggable targets for erlotinib-resistant lung cancer

Project description:This study aims to identify new genes and pathways associated with erlotinib sensitivity in order to develop novel therapeutic strategies. Here, we induced artificial knock-out (KO) mutations in erlotinib-resistant human lung cancer cells (NCI-H820) using a genome-scale CRISPR-Cas9 sgRNA library to screen for genes involved in erlotinib susceptibility.

2020-11-30 | GSE142669 | GEO

Genome-scale CRISPR screening identifies cell cycle and protein ubiquitination processes as druggable targets for erlotinib-resistant lung cancer.

Project description: Not available

| S-EPMC7858278 | biostudies-literature

Differential Gene Expression in Erlotinib-Treated Fibroblasts

Project description:Analysis of human, adult, dermal fibroblasts following treatment with 100nM or 1 uM of erlotinib, a tryrosine kinase inhibitor (TKI) that targets the epidermal growth factor receptor (EGFR) inhibiting EGFR activation and signaling. Erlotinib is widely used to effectively treat patients with advanced non-small cell lung cancer but treatment with erlotinib and other EGFR TKIs are associated with a painful skin rash. Results identified significantly differentially expressed genes in fibroblasts treated with erlotinib providing insight into how the drug alters the transcriptome in ways that may contribute to the TKI-related rash.

2019-01-01 | GSE106151 | GEO

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.

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

2014-10-07 | E-GEOD-62118 | biostudies-arrayexpress

Differential microRNA Expression in USP8-Mutated and Wild-Type Corticotroph Pituitary Tumors Reflect the Difference in Protein Ubiquitination Processes

Project description:Background: USP8 mutations are the most common driver changes in corticotroph pituitary tumors. They have direct effect on cells’ proteome through disturbance of ubiquitination process and also influence gene expression. The aim of this study was to compare microRNA profiles in USP8- mutated and wild-type tumors and determine the probable role of differential microRNA expression by integrative microRNA and mRNA analysis. Methods: Patients with Cushing’s disease (n = 28) and silent corticotroph tumors (n = 20) were included. USP8 mutations were identified with Sanger sequencing. MicroRNA and gene expression was determined with next-generation sequencing. Results: USP8-mutated patients with Cushing’s disease showed higher rate of clinical remission and trend towards lower tumor volume than wild-type patients. Comparison of microRNA profiles of USP8-mutated and wild-type tumors revealed 68 differentially expressed microRNAs. Their target genes were determined by in silico prediction and microRNA/mRNA correlation analysis. GeneSet Enrichment analysis of putative targets showed that the most significantly overrepresented genes are involved in protein ubiquitination-related processes. Only few microRNAs influence the expression of genes differentially expressed between USP8-mutated and wild-type tumors. Conclusions: Differences in microRNA expression in corticotropinomas stratified according to USP8 status reflect disturbed ubiquitination processes, but do not correspond to differences in gene expression between these tumors.

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

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Gene expression profiling of generated Erlotinib-resistant (ER) cell lines

Project description:Targeted therapies have provided advantages to cancer patients, but these therapies are limited by differential responses and developed resistance. To discover mechanisms of resistance, we developed drug-resistant cell lines and have their gene expressions profiled and compared. HCC827 cells, which were initially sensitive to Erlotinib treatment, are subjected to Erlotinib treatment. Two clonal populations that resistant to Erlotinib resulted.

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