Transcriptional profiling of mouse ovarian surface epithelial cells during in vitro spontaneous transformation
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE81729 | GEO | 2016/11/16
SECONDARY ACCESSION(S): PRJNA322449
REPOSITORIES: GEO
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Project description:Ovarian cancer is one of the most deadly cancers accounting for only 3% of diagnosed cancers, but is the fifth leading cause of cancer deaths among woman; however, the progression of ovarian cancer is poorly understood. To study and further understand the early events that lead to epithelial derived ovarian cancer, we previously developed a cell model of progressive ovarian cancer. Mouse ovarian surface epithelial (MOSE) cells have undergone spontaneous transformation in cell culture and represent pre-neoplastic, non-tumorigenic to an aggressive malignant phenotype. Microarray analysis was performed with RNA isolated from different stages of MOSE cells to examine changes in gene expression as MOSE cells transition from a pre-neoplastic to a malignant state. RNA was isolated from MOSE early cell representing a pre-neoplastic, non-malignant stage, MOSE Intermediate cells representing a noeplastic, pre-invasive state, and MOSE Late cells representing a malignant, invasive stage. Three biological replicates were used to take into account variations within the heterogeneous cultures.
2011-03-03 | E-GEOD-24789 | biostudies-arrayexpress
Project description:Ovarian cancer is one of the most deadly cancers accounting for only 3% of diagnosed cancers, but is the fifth leading cause of cancer deaths among woman; however, the progression of ovarian cancer is poorly understood. To study and further understand the early events that lead to epithelial derived ovarian cancer, we previously developed a cell model of progressive ovarian cancer. Mouse ovarian surface epithelial (MOSE) cells have undergone spontaneous transformation in cell culture and represent pre-neoplastic, non-tumorigenic to an aggressive malignant phenotype. Microarray analysis was performed with RNA isolated from different stages of MOSE cells to examine changes in gene expression as MOSE cells transition from a pre-neoplastic to a malignant state.
2011-03-03 | GSE24789 | GEO
Project description:Our lab established the M0505 cell line from the ovarian surface epithelium (OSE) of FVB/N mice in May 2005 in order to study OSE biology. This cell line was infected with PAX2 to study the biological consequences of PAX2 expression in normal mOSE cells We used microarrays to try to determine the downstream targets of PAX2 in mOSE (M0505) cells to gain information that may lead to a greater understanding of its oncongenic potential.
2015-05-27 | GSE69238 | GEO
Project description:Our lab established the M0505 cell line from the ovarian surface epithelium (OSE) of FVB/N mice in May 2005 in order to study OSE biology. This cell line was infected with PAX2 to study the biological consequences of PAX2 expression in normal mOSE cells We used microarrays to try to determine the downstream targets of PAX2 in mOSE (M0505) cells to gain information that may lead to a greater understanding of its oncongenic potential. Two biological replicates of M0505+WPI, M0505+PAX2 and M0505+PAX2+Cre cells were collected for RNA extraction and subesequent hybridization on the Affymetrix MoGene-1_0-st-v1 platform.
2015-05-27 | E-GEOD-69238 | biostudies-arrayexpress
Project description:Most ovarian cancers originate from the ovarian surface epithelium and are characterized by aneuploid karyotypes. Aneuploidy, a consequence of chromosome instability, is an early event during the development of ovarian cancers. However, how aneuploid cells are evolved from normal diploid cells in ovarian cancers remains unknown. In the present study, cytogenetic analyses of a mouse syngeneic ovarian cancer model revealed that diploid mouse ovarian surface epithelial cells (MOSECs) experienced an intermediate tetraploid cell stage, before evolving to aneuploid (mainly near-tetraploid) cells. Using long-term live-cell imaging followed by fluorescence in situ hybridization (FISH), we demonstrated that tetraploid cells originally arose from cytokinesis failure of bipolar mitosis in diploid cells, and gave rise to aneuploid cells through chromosome mis-segregation during both bipolar and multipolar mitoses. Injection of the late passage aneuploid MOSECs resulted in tumor formation in C57BL/6 mice. Therefore, we reveal a pathway for the evolution of diploid to aneuploid MOSECs and elucidate a mechanism for the development of near-tetraploid ovarian cancer cells.
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Project description:Developmental differences in gene expression in the postnatal mouse cochlear nucleus was analyzed at two or three ages using two different array platforms, the Affymetrix Mouse 430A GeneChip or the NIA 15K mouse cDNA microarray. These ages, P7, P14, and P21 parallel a critical period of neuron survival dependent on input from the auditory nerve. Keywords: parallel sample
2005-10-15 | GSE2390 | GEO
Project description: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?<?0.05) comprised 7 genes coding for centralspindlin, chromosome passenger and minichromosome maintenance protein complexes. The genes Ccnb1 (Cyclin B1), Birc5 (Survivin), Nusap1 and Kif23 were the most recurrent in over a dozen GO terms related to the mitotic process. On the other hand, Pten plus the large non-coding RNAs Malat1 and Neat1 were among the 80 down-regulated genes with mRNA processing, nuclear bodies, ER-stress response and tumor suppression as relevant terms. Interestingly, the earliest discrete segmental aneuploidies arose by passage 18 in chromosomes 7, 10, 11, 13, 15, 17 and 19. By passage 23, when MOSE cells express the malignant phenotype, the dysregulated gene expression repertoire expanded, DNA imbalances enlarged in size and covered additional loci.Prior to early aneuploidies, overexpression of genes coding for the mitotic apparatus in passage-14 pre-malignant MOSE cells indicate an increased proliferation rate suggestive of replicative stress. Concomitant down-regulation of nuclear bodies and RNA processing related genes suggests altered control of nuclear RNA maturation, features recently linked to impaired DNA damage response leading to genome instability. These results, combined with cytogenetic analysis by other authors in this model, suggest that transcriptional profile at passage 14 might induce cytokinesis failure by which tetraploid cells approach a near-tetraploid stage containing primary chromosome aberrations that initiate the tumorigenic drive.
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Project description:Liver and BAT expression differences between the fat F-line, and congenic Fob3b-line. Normalised data appended as follows: TABLE 1: LIVER - 1st set (7.5K) of the 2 slide NIA NIH 15K set -source1 = F-line liver male - 2 pools each made from 5 different individuals -source2 = Fob3b-line (aka Fchr15D-line) liver male - 2 pools each made from 5 different individuals -values are normalised using mixed model across 6 slides: 1 F-line vs Fline 2 Fob3b-line vs Fob3b-line 3 F-line pool1 vs Fob3b-line pool1 4 F-line pool1 vs Fob3b-line pool1 -dye swap 5 F-line pool2 vs Fob3b-line pool2 6 F-line pool2 vs Fob3b-line pool2 -dye swap TABLE 2: LIVER - 2nd set (7.5K) of the 2 slide NIA NIH 15K set -source1 = F-line liver male - 2 pools each made from 5 differnt individuals -source2 = Fob3b-line (aka Fchr15D-line) liver male - 2 pools each made from 5 differnt individuals -values are normalised using mixed model across 6 slides: 1 F-line Vs F-line 2 Fob3b-line vs Fob3b-line 3 F-line pool1 vs Fob3b-line pool2 4 F-line pool1 vs Fob3b-line pool2 dye swap 5 F-line pool2 vs Fob3b-line pool1 6 F-line pool2 vs Fob3b-line pool1 dye swap TABLE 3: Brown Adipose Tissue (BAT) 1st (7.5K) array set of 15K NIA NIH set -source1 = F-line male BAT from 2 pools each made from 5 different individuals -source2 = Fob3b-line (aka Fchr15D-line) male BAT from 2 pools each made from 5 different individuals -values are normalised using mixed model across 4 slides: 1 F-line pool1 vs Fob3b-line pool1 2 F-line pool1 vs Fob3b-line pool1 dye swap 3 F-line pool2 vs Fob3b-line pool2 4 F-line pool2 vs Fob3b-line pool2 dye swap TABLE 4: Brown Adipose Tissue (BAT) 2nd (7.5K) array of the 15K NIA NIH set -source1 = F-line male BAT (2 pools each from 5 individual mice) -source2 = Fob3b-line (aka Fchr15D-line) male BAT (2 pools each from 5 individual mice) -values are normalised using mixed model across 4 slides: 1 F-line pool1 vs Fob3b-line pool1 2 F-line pool1 vs Fob3b-line pool1 dye swap 3 F-line pool2 vs Fob3b-line pool2 4 F-line pool2 vs Fob3b-line pool2 dye swap Keywords = Obesity Keywords = Fob3b Keywords = QTL Keywords = congenic Keywords: other
2004-12-16 | GSE1558 | GEO
Project description:Global transcriptomic analysis of murine ovarian surface epithelial (MOSE) cells with PAX8 overexpression
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