Dysregulation of mitotic machinery genes precedes genome instability during spontaneous pre-malignant transformation of mouse ovarian surface epithelial cells

Based in epidemiological evidence, repetitive ovulation has been proposed to play a role in the origin of ovarian cancer by inducing an aberrant wound rupture-repair process of the ovarian surface epithelium (OSE). Accordingly, long term cultures of isolated OSE cells undergo in vitro spontaneous tr...

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Bibliographic Details
Published in:BMC genomics 2016-10, Vol.17 (Suppl 8), p.728-728, Article 728
Main Authors: Urzúa, Ulises, Ampuero, Sandra, Roby, Katherine F, Owens, Garrison A, Munroe, David J
Format: Article
Language:English
Subjects:
Aneuploidy
Animals
Cell Transformation, Neoplastic - genetics
Cell Transformation, Neoplastic - metabolism
Comparative Genomic Hybridization
Development and progression
DNA Copy Number Variations
DNA microarrays
Epithelial Cells - metabolism
Epithelial Cells - pathology
Female
Gene Expression Profiling
Gene Expression Regulation
Gene Regulatory Networks
Genetic aspects
Genetic regulation
Genome
Genomic Instability
Mice
Mitosis - genetics
Mouse ovarian surface epithelium
Ovarian cancer
Ovarian cancer model
Ovarian Neoplasms - genetics
Ovarian Neoplasms - metabolism
Ovarian Neoplasms - pathology
Ovary - metabolism
Phenotype
Physiological aspects
Precancerous Conditions - genetics
Preneoplasia
Protein Interaction Maps
Transcriptome
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Summary:Based in epidemiological evidence, repetitive ovulation has been proposed to play a role in the origin of ovarian cancer by inducing an aberrant wound rupture-repair process of the ovarian surface epithelium (OSE). Accordingly, long term cultures of isolated OSE cells undergo in vitro spontaneous transformation thus developing tumorigenic capacity upon extensive subcultivation. In this work, C57BL/6 mouse OSE (MOSE) cells were cultured up to passage 28 and their RNA and DNA copy number profiles obtained at passages 2, 5, 7, 10, 14, 18, 23, 25 and 28 by means of DNA microarrays. Gene ontology, pathway and network analyses were focused in passages earlier than 20, which is a hallmark of malignancy in this model. At passage 14, 101 genes were up-regulated in absence of significant DNA copy number changes. Among these, the top-3 enriched functions (>30 fold, adj p 
ISSN:1471-2164
1471-2164
DOI:10.1186/s12864-016-3068-5