Project description:To investigate the roles of TAZ in lung cancer cell proliferation, we compared the expression profiles of A549 and H441 lung adenocarcinoma cell lines transfected with control siRNA and siTAZ.
Project description:To investigate the roles of TAZ in lung cancer cell proliferation, we compared the expression profiles of A549 and H441 lung adenocarcinoma cell lines transfected with control siRNA and siTAZ. We collected RNA from A549 and H441 cell lines transfected with control siRNA and siTAZ.
Project description:To identify differentially expressed genes by miRNAs transfection in human cancer, several cell lines (lung adenocarcinoma, lung squamous cell carcinoma and small cell lung cancer) were subjected to Agilent whole genome microarrays.
Project description:FDFT1 catalyzes the first reaction in the mevalonate/isoprenoid pathway, we demonstrated that FDFT1 down-regulation by two shRNAs significantly reduced cell migration and invasion in highly invasive lung cancer cell lines in vitro, as well as in lung metastases in vivo. We used microarrays to detail the FDFT1 regulated gene expression underlying invasion-metastasis cascade and identified distinct classes of up-regulated genes during this process. Lung adenocarcinoma cells with FDFT1 overexpression were selected for RNA extraction and hybridization on Affymetrix microarrays.
Project description:In addition to the generation and analysis of metabolomics data on cell lines, samples of normal lung tissue, adenocarcinoma lung tissue and small cell lung carcinoma tissue (seven samples/group) were processed and evaluated metabolite profile differences under the scope of the pilot and feasibility study. These data can be correlated to the metabolite profiles defined in the SCLC and NSCLC cell lines and integrated with the ABPP-determined metabolic kinases to identify distinct metabolic signatures or biomarkers (?oncometabolites?) that distinguish small cell lung cancer from non-small cell lung cancer.
Project description:The NKX2-1 transcription factor, a regulator of normal lung development, is the most significantly amplified gene in human lung adenocarcinoma. To better understand how genomic alterations of NKX2-1 drive tumorigenesis, we generated an expression signature associated with NKX2-1 amplification in human lung adenocarcinoma, and analyzed DNA binding sites of NKX2-1 by genome-wide chromatin immunoprecipitation from NKX2-1-amplified human lung adenocarcinoma cell lines. Combining these expression and cistromic analyses identified LMO3, itself encoding a transcription regulator, as a candidate direct transcriptional target of NKX2-1, in addition to consensus binding motifs including a nuclear hormone receptor signature and a Forkhead box motif in NKX2-1-bound sequences. RNA interference analysis of NKX2-1-amplified cells compared to non-amplified cells demonstrated that LMO3 mediates cell proliferation downstream of NKX2-1; cistromic analysis that NKX2-1 may cooperate with FOXA1. Our findings provide new insight into the transcriptional regulatory network of NKX2-1 and suggest that LMO3 is a transducer of lineage specific cell survival of NKX2-1-amplified lung adenocarcinomas. NKX2-1 ChIP-seq from three lung adenocarcinoma cell lines with amplification of NKX2-1