Transcriptome in NSCLC cell lines
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA808994 | ENA |
REPOSITORIES: ENA
Similar Datasets
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Project description:34 NSCLC cell lines were transcriptionally profiled against a reference mix of 45 NSCLC cell lines to look subtype specific differential gene expression
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Project description:Protein glycosylation plays a fundamental role in a multitude of biological processes, and the associated aberrant expression of glycoproteins in cancer has made them attractive targets as biomarkers and therapeutic targets. In this study, we examined differentially expressed glycoproteins in cell lines derived from three different states of lung tumorigenesis: an immortalized bronchial epithelial cell (HBE) line, a non-small cell lung cancer (NSCLC) cell line harboring an activation KRAS mutation and a NSCLC cell line harboring an EGFR activation deletion. Mutations in KRAS and EGFR are two common, distinct, non-overlapping genomic alterations in NSCLC. Using a Triple SILAC proteomic quantification strategy paired with hydrazide chemistry N-linked glycopeptide enrichment, we identified 118 quantifiable glycopeptides in the 3 cell lines derived from 82 glycoproteins. Proteomic profiling revealed that 27 (24%) of the glycopeptides overexpressed in both of the NSCLC cell lines with 6 of the glycopeptides overexpressed only in the EGFR mutant cells and 19 of the glycopeptides overexpressed only in the KRAS mutant cells.
2015-12-10 | PXD001999 | Pride
Project description:Protein glycosylation plays a fundamental role in a multitude of biological processes, and the associated aberrant expression of glycoproteins in cancer has made them attractive targets as biomarkers and therapeutic targets. In this study, we examined differentially expressed glycoproteins in cell lines derived from three different states of lung tumorigenesis: an immortalized bronchial epithelial cell (HBE) line, a non-small cell lung cancer (NSCLC) cell line harboring an activation KRAS mutation and a NSCLC cell line harboring an EGFR activation deletion. Mutations in KRAS and EGFR are two common, distinct, non-overlapping genomic alterations in NSCLC. Using a Triple SILAC proteomic quantification strategy paired with hydrazide chemistry N-linked glycopeptide enrichment, we identified 118 quantifiable glycopeptides in the 3 cell lines derived from 82 glycoproteins. Proteomic profiling revealed that 27 (24%) of the glycopeptides overexpressed in both of the NSCLC cell lines with 6 of the glycopeptides overexpressed only in the EGFR mutant cells and 19 of the glycopeptides overexpressed only in the KRAS mutant cells.
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Project description:<p>We have used a "chemistry first" approach to discover druggable acquired vulnerabilities that arised in the pathogenesis of non-small cell lung cancer (NSCLC). We screened chemical libraries (~200,000 compounds) for chemical toxins that killed subsets of NSCLC but not normal human lung epithelial cells (HBECs). We first screened a panel of 12 NSCLC lines that represented a variety of known oncogenotypes and identified chemicals with large Z scores and appropriate properties including re-supply, chemistry, and reproducible drug response phenotypes. This was then narrowed down to a list of 202 chemicals and 18 drugs with known targeting (henceforth called "Precision Oncology Probe Set", or POPS). These, and a panel of 30 clinically available drugs, targeted therapies, and drug combinations, already in use or in trials for NSCLC treatment, were then tested on a panel of 96 NSCLC lines for their drug response phenotypes in 12-point dose response curves. This information was analyzed using scanning ranked KS (Kolmogorov-Smirnov) and elastic net biostatistics approaches to identify molecular biomarkers (mutations, mRNA expression, copy number variation, protein expression, and metabolomics) which could predict for sensitivity or resistance to a particular chemical toxin or treatment regimen. From this we have discovered that: our approach identifies already known molecular biomarker of drug sensitivities (e.g. EGFR mutations and EGFR TK inhibitors); many clinically available chemotherapy agents have molecular biomarkers predicting preclinical model drug responses; the POP set of chemical toxins provides novel drug response phenotype patterns in the large NSCLC panel different from those found with clinically available agents including a therapeutic window; many of the POP toxins only hit a small percentage (~5%) of the NSCLC panel but the POP set as a whole provides "coverage" of the entire NSCLC panel; there are simple, one or 2 component molecular biomarkers (mutations, mRNA expression) that predict responses to the different chemical toxins in the NSCLC panel; and that the molecular biomarkers provide some information on the targets and pathways involved in response to the chemical toxins. Thus, we have identified a group of chemical toxins with selectivity for subsets of NSCLC and associated tumor molecular biomarkers to facilitate their development for precision medicine, and also, in some cases, information on the targets and pathways interdicted by these chemical compounds. In addition, we have discovered NSCLC predictive biomarkers for clinically available agents.</p>
| phs001823 | dbGaP