Project description:Transcriptional profiling of two human lung cancer cell lines, DMS-273 (small cell lung cancer) and NCI-H1437 (non-small cell lung cancer), stably transfected either with innocuous scrambled shRNAs or SETDB1-specific.The objective was to identify global gene expression changes due to the depletion of the H3K9me3 methyltransferase SETDB1. 3 replicates for DMS-273 and 1 Control; 2 replicates for NCI-H1437 and 1 Control
Project description:Transcriptional profiling of two human lung cancer cell lines, DMS-273 (small cell lung cancer) and NCI-H1437 (non-small cell lung cancer), stably transfected either with innocuous scrambled shRNAs or SETDB1-specific.The objective was to identify global gene expression changes due to the depletion of the H3K9me3 methyltransferase SETDB1.
Project description:To explore how PKCδ regulates tumorigenesis, we performed mRNA expression analysis of four KRAS mutant NSCLC cell lines that stably express scrambled shRNA or PKCδ targeted shRNA
Project description:To explore how PKCδ regulates tumorigenesis, we performed mRNA expression analysis of four KRAS mutant NSCLC cell lines that stably express scrambled shRNA or PKCδ targeted shRNA Four human lung cancer cell lines (A549, H441, H460 and H2009) with scrambled and PKC-delta knock down (shRNA), in triplicate.
Project description:PTK7 was identified from a meta-analysis of 1905 non-small-cell lung cancer (NSCLC) samples across 12 datasets to be one of seven genes commonly up-regulated in lung adenocarcinoma (ADC). Using ADC cell lines NCI-H1299 and NCI-H2009, disruption of PTK7 resulted in decreased cell viability and induction of apoptosis. A xenotransplantation model of the cell lines with PTK7 knock-down also resulted in decreased tumor burden. We assayed gene expression in these cell lines after PTK7 knock-down by shRNA to uncover deregulated pathways and genes.
Project description:PTK7 was identified from a meta-analysis of 1905 non-small-cell lung cancer (NSCLC) samples across 12 datasets to be one of seven genes commonly up-regulated in lung adenocarcinoma (ADC). Using ADC cell lines NCI-H1299 and NCI-H2009, disruption of PTK7 resulted in decreased cell viability and induction of apoptosis. A xenotransplantation model of the cell lines with PTK7 knock-down also resulted in decreased tumor burden. We assayed gene expression in these cell lines after PTK7 knock-down by shRNA to uncover deregulated pathways and genes. 8 samples were analyzed. In each cell line, we knocked down PTK7 with 2 independent hairpins, and 2 control hairpins targeting luciferase and GFP. Thus, NCI-H1299 has 2 samples of PTK7 knock-down, and 2 samples of control knock down. NCI-H2009 has similar samples.
Project description:To determine miRNAs regulated by TTF-1 in SCLC cell lines, miRNA array analyses were carried out in NCI-H209 cells following TTF-1 knockdown
Project description:This is a Dose response experiment carried out using the BET inhibitor JQ1 in SCLC cell lines. Approximately 1x106 cells of cell lines, DMS-53, H69, H1694, H1048, H2227 were treated for 2 hours with a 12 point dose range of JQ1 (7500nM to 0.04nM). Lysates were collected at the end of the treatment in 300ul TRI reagent for RNA preparation for expression profiling.
Project description:The study was designed to identify the molecular changes that occur in EGFR mutant NSCLCs that become resistant to TKI by transforming to SCLC. Tyrosine kinase inhibitors (TKIs) are effective treatments for non-small cell lung cancers (NSCLCs) with epidermal growth factor receptor (EGFR) mutations. However, they do not lead to cures, and, on average, relapse occurs after one year of continuous treatment. In a subset of patients, a fundamental histological transformation from NSCLC to small cell lung cancer (SCLC) is observed in the resistant cancers, but the molecular changes associated with this transformation remain unknown. Analysis of a cohort of tumor samples and cell lines derived from resistant EGFR mutant patients with SCLC transformation revealed that RB is lost in 100% of these cases, but rarely in those that remain NSCLC. Global changes in gene expression, including increased neuroendocrine marker expression and absence of EGFR expression, are observed in cancers that transformed to SCLC. Consistent with their genetic and epigenetic similarities to classical SCLC, cell lines derived from resistant EGFR mutant SCLC biopsies are substantially more sensitive to ABT-263 treatment compared to those derived from resistant EGFR mutant NSCLCs. Together, these findings suggest that despite developing initially as EGFR mutant adenocarcinomas, this subset of resistant cancers ultimately take on many of the molecular and phenotypic characteristics of classical SCLC. Overall, we completed array CGH analysis on 4 tumor specimens from EGFR mutant, TKI-resistant patients. Three of these samples had transformed to SCLC and one remained NSCLC.
