3' UTR RNA-seq of EGFR-mutant PC9 cells and drug-resistant clones
Ontology highlight
ABSTRACT: EGFR-mutant lung adenocarcnioma cell line PC9 pools were treated with different compounds until resistant cells regrew. Resistant and parental cells were then sequenced to study transcriptional changes.
Project description:Lung adenocarcinoma PC9 cells were engineered to not only contain the driving EGFR-mutations, but also EGFR T790M and EGFR C797S that provide resistance to EGFR inhibitors.
Project description:Human EGFR-mutant lung adenocarcinoma cells (PC9) were engineered using CRISPRv2 systemt to knock-out MAVS or STING to assess impact on transcriptomic response following osimertinib treatment
Project description:Drug tolerant persister cells of EGFR-mutant PC9 cell lines surviving treatment with kinase inhibitor combination. Cells were treated with combination of erlotinib, osimertinib, trametinib and dasatinib and surviving cells were harvested for RNA extraction. 3' UTR RNA-seq profiles were compared to parental control cells and to outgrowing cells after treatment had been removed
Project description:Immunocompromised mice were inoculated with human lung adenocarcinoma cell line PC9 and with human PBMCs. Tumors were treated with osimertinib/vehicle of RIG-I agonist IVT4/unspecific control IVT-GAC to assess response.
Project description:Human EGFR-mutated lung adenocarcinoma cell lines HCC4006, HCC827 and PC9 were treated with trametinib or DMSO to assess the impact on transcription.
Project description:In the human EGFR mutant adenocarcinoma cell line PC9 pBabe empty vector (EV) or BRAF V600E were overexpressed. RNA was extracted from EV, BRAF V600E overexpressing or osimertinib-resistant BRAF V600E expressing cells after 48h treatment with osimertinib, trametinib, a combination of both or vehicle controls. RNA was subjected to 3' UTR RNA sequencing.
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.
Project description:To investigate the possible resistant mechanism to osimertinib, PC9 cells and their derived osimertinib-resistant PC9OR cells were sequenced using illumina HiSeq. We then performed gene expression profiling analysis using data obtained from RNA-seq of PC9 cells and their derived PC9OR cells.
Project description:The goals of this study are to compare the different transcriptome signiture between PC9 and MTAC-P with NGS-derived retinal transcriptome profiling (RNA-seq).