Project description:ETS2 is a canonical transcriptional factor and member of the ETS family of genes. ETS2 binds to consensus ERE binding sites in a broad spectrum of genes thus affecting many intracellular molecular functions. However, the role of ETS2 in the biology and pathogenesis of lung cancers is still not known. We have found that ETS2 is down-regulated in lung tumors compared to normal lung tissue and the expression of the coding protein of the gene was a significant independent predictor of favorable outcome in NSCLC patients pinpointing to a potential tumor suppressor role for this gene. To better understand its molecular function in NSCLC, we compared and contrasted the transcriptome of lung cancer cells transfected with control siRNA and siRNA targeting ETS2. H441 lung cancer cells were transfected with SMARTpool (Dharmacon)control/scrambled siRNA or siRNA targeting ETS2. Three independent transfections were performed cells with control siRNA and for cells with siRNA specific to ETS2 where each transfection consittutes a biological replicate. Knock-down of ETS2 in all samples was confirmed by quantitative real-time PCR. Total RNA was then profiled using the Human Gene
Project description:ETS2 is a canonical transcriptional factor and member of the ETS family of genes. ETS2 binds to consensus ERE binding sites in a broad spectrum of genes thus affecting many intracellular molecular functions. However, the role of ETS2 in the biology and pathogenesis of lung cancers is still not known. We have found that ETS2 is down-regulated in lung tumors compared to normal lung tissue and the expression of the coding protein of the gene was a significant independent predictor of favorable outcome in NSCLC patients pinpointing to a potential tumor suppressor role for this gene. To better understand its molecular function in NSCLC, we compared and contrasted the transcriptome of lung cancer cells transfected with control siRNA and siRNA targeting ETS2.
Project description:Gene expression data were collected by RNA-seq from HCT-116 cells in the presence or absence of siRNA targeting APC and 1,376 transcripts changed in expression following APC silencing were identified relative to scrambled siRNA-transfected and untreated controls.
Project description:Transcriptional profiling for global characterization of gene expression alterations that resulted from treatment of melanoma cells with siRNA specifically targeting NRASQ61R Experiment Overall Design: BL or 224 cells transfected with siRNA against either mutant NRASQ61R (siMut10 and siMut12) or scrambled control (siSC). Untransfected cells (T0) from Day 0 were used as the baseline control for cells transfected with both siMut and siSC
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:Transcriptional profiling of HT-29 human colon cancer cells transfected with non-targeting control (NTC) siRNA and two different siRNA sequences against CDK8 (siCDK8-1 and siCDK8-2).
Project description:Primary murine lung fibroblasts were transfected with either control (scrambled) or sequence-specific siRNA against Lysyl oxidase (Lox), Lysyl oxidase-like (Loxl1) or Lysyl oxidase-like 2 (Loxl2) genes. Cells were harvested 48 hours after the transfection. Multiple changes in gene expression were found in the corrected p values in this microarray study.
Project description:We recently characterized the adjacent airway field of cancerization in NSCLC by whole transcriptome expression analysis and demonstrated that lysosomal protein transmembrane 4 beta (LAPTM4B) was an elevated field cancerization marker in NSCLCs and in adjacent but not in distant normal-appearing airways. We also found that LAPTM4B was up-regulated in NSCLCs compared to normal lung and promoted anchorage-dependent growth of lung cancer cells. Previous reports suggested that LAPTM4B is activated following metabolic and genotixc stress. The precise role of LAPTM4B in lung cancer cell survival and NSCLC pathogenesis is still elusive. In the present study we sought to examine how LAPTM4B expression levels impact downstream expression profiles and cell signaling in order to gain better insights into the function of this putative oncogene in lung cancer. Calu-6 lung cancer cells were transfected with SMARTpool (Dharmacon)control/scrambled siRNA or siRNA targeting LAPTM4B. Following transfection, cells were cultured in the presence or absence of 10% fetal bovine serum (FBS). Three independent transfections for each condition were performed representing three biological replicates per condition (total number of samples = 12). RNA interference-mediated knock-down of LAPTM4B in samples was confirmed by quantitative real-time PCR. Total RNA was profiled using the Human Gene 1.0 ST platform.