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Aneuploidy, oncogene amplification, and epithelial to mesenchymal transition define spontaneous transformation of murine epithelial cells [CGH]

ABSTRACT: Human epithelial cancers are defined by a recurrent distribution of specific chromosomal aneuploidies. In our model system, mouse bladder and kidney epithelial cells spontaneously immortalize, transform and become tumorigenic after prolonged culture. We assessed genome and transcriptome alterations and found wide-spread aneuploidy, early transcriptional deregulation, and massive genomic dereguation of the cellular transcriptome. The results reveal a remarkable similarity with genome and transcriptome aberrations detected in human tumorigenesis, hence validating our newly derived cancer models.

ORGANISM(S): Mus musculus

PROVIDER: GSE45128 | GEO | 2013/03/14

SECONDARY ACCESSION(S): PRJNA192940

REPOSITORIES: GEO

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Aneuploidy, oncogene amplification, and epithelial to mesenchymal transition define spontaneous transformation of murine epithelial cells [transcriptome]

2013-03-14 | GSE45127 | GEO

Aneuploidy, oncogene amplification, and epithelial to mesenchymal transition define spontaneous transformation of murine epithelial cells [transcriptome]

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2013-03-14 | E-GEOD-45127 | biostudies-arrayexpress

Aneuploidy, oncogene amplification, and epithelial to mesenchymal transition define spontaneous transformation of murine epithelial cells [CGH]

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Project description:Aneuploidy, or an aberrant karyotype, results in developmental disabilities and has been implicated in tumorigenesis. However, the causes of aneuploidy-induced phenotypes and the consequences of aneuploidy on cell physiology remain poorly understood. We have performed a meta-analysis on gene expression data from aneuploid cells in diverse organisms, including yeast, plants, mice, and humans. We found highly-related gene expression patterns that are conserved between species: genes that were involved in the response to stress were consistently upregulated, while genes associated with the cell cycle and cell proliferation were downregulated in aneuploid cells. Within species, different aneuploidies induced similar changes in gene expression, independent of the specific chromosomal aberrations. Taken together, our results demonstrate that aneuploidies of different chromosomes and in different organisms impact similar cellular pathways and cause a stereotypical anti-proliferative response that must be overcome prior to transformation. These experiments are two-color hybridizations of RNA isolated from aneuploid samples vs matched wt cells, all grown to midlog phase.

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2010-02-24 | E-GEOD-20464 | biostudies-arrayexpress

Loss of the SUMO Protease Ulp2 Triggers a Specific Multi-Chromosome Aneuploidy

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