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  • GENES  (2)
  • 1
    Keywords: CANCER ; GROWTH ; INHIBITOR ; proliferation ; SURVIVAL ; tumor ; CELL-PROLIFERATION ; Germany ; KINASE ; INFORMATION ; TOOL ; DISEASE ; GENE ; GENES ; GENOME ; microarray ; PROTEIN ; PROTEINS ; transcription ; TUMORS ; RESOLUTION ; ACTIVATION ; DNA ; BIOLOGY ; cell cycle ; CELL-CYCLE ; CYCLE ; ASSOCIATION ; MOUSE ; IDENTIFICATION ; PROGRESSION ; ASSAY ; microarrays ; PROSTATE-CANCER ; STRATEGIES ; DNA-REPLICATION ; REPLICATION ; signaling ; RE ; TUMORIGENICITY ; genomics ; TRANSITION ; DNA replication ; C-ELEGANS ; cell proliferation ; PROTEIN-ANALYSIS ; development ; ASSAYS ; DIFFERENTIALLY EXPRESSED GENES ; high throughput ; HIGH-THROUGHPUT ; LONG ; PRIME ; PRINCIPLES ; REPRESSOR ; ROLES
    Abstract: Cancer transcription microarray studies commonly deliver long lists of "candidate" genes that are putatively associated with the respective disease. For many of these genes, no functional information, even less their relevance in pathologic conditions, is established as they were identified in large-scale genomics approaches. Strategies and tools are thus needed to distinguish genes and proteins with mere tumor association from those causally related to cancer. Here, we describe a functional profiling approach, where we analyzed 103 previously uncharacterized genes in cancer relevant assays that probed their effects on DNA replication (cell proliferation). The genes had previously been identified as differentially expressed in genome-wide microarray studies of tumors. Using an automated high-throughput assay with single-cell resolution, we discovered seven activators and nine repressors of DNA replication. These were further characterized for effects on extracellular signal-regulated kinase 1/2 (ERK1/2) signaling (G(1)-S transition) and anchorage-independent growth (tumorigenicity). One activator and one inhibitor protein of ERK1/2 activation and three repressors of anchorage-independent growth were identified. Data from tumor and functional profiling make these proteins novel prime candidates for further in-depth study of their roles in cancer development and progression. We have established a novel functional profiling strategy that links genomics to cell biology and showed its potential for discerning cancer relevant modulators of the cell cycle in the candidate lists from microarray studies
    Type of Publication: Journal article published
    PubMed ID: 16140941
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  • 2
    Keywords: SURVIVAL ; CELL ; Germany ; MICROSCOPY ; screening ; GENE ; GENES ; GENOME ; RNA ; IDENTIFICATION ; ARRAYS ; HUMAN GENOME ; MIGRATION ; PHENOTYPE ; ORGANIZATION ; INTERFERENCE ; RNA INTERFERENCE ; RESOURCE ; SCIENCE ; LIFE ; TISSUE-CULTURE CELLS
    Abstract: Despite our rapidly growing knowledge about the human genome, we do not know all of the genes required for some of the most basic functions of life. To start to fill this gap we developed a high-throughput phenotypic screening platform combining potent gene silencing by RNA interference, time-lapse microscopy and computational image processing. We carried out a genome-wide phenotypic profiling of each of the similar to 21,000 human protein-coding genes by two-day live imaging of fluorescently labelled chromosomes. Phenotypes were scored quantitatively by computational image processing, which allowed us to identify hundreds of human genes involved in diverse biological functions including cell division, migration and survival. As part of the Mitocheck consortium, this study provides an in-depth analysis of cell division phenotypes and makes the entire high-content data set available as a resource to the community
    Type of Publication: Journal article published
    PubMed ID: 20360735
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