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The gene profile analysis of the function of HMGA2 in immortalized human ovarian surface epithelial cell lines.

ABSTRACT: To identify HMGA2-regulated downstream target genes, we compared the difference of gene profiles between ovarian surface epithelial cells without HMGA2 (T29-1, T29-2, T80) and cells with HMGA2 (T29A2-8, T29A2-15, T80A2-11).

ORGANISM(S): Homo sapiens

PROVIDER: GSE23599 | GEO | 2010/08/14

SECONDARY ACCESSION(S): PRJNA131743

REPOSITORIES: GEO

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The gene profile analysis of the function of HMGA2 in immortalized human ovarian surface epithelial cell lines.

Project description:To identify HMGA2-regulated downstream target genes, we compared the difference of gene profiles between ovarian surface epithelial cells without HMGA2 (T29-1, T29-2, T80) and cells with HMGA2 (T29A2-8, T29A2-15, T80A2-11). Immortalized ovarian surface epithelial cells (named T29-1, T29-2, T80) were transfected with HMGA2 retrovirus vector pBabe-HMGA2 (named T29A2-8, T29A2-15, T80A2-11). Then cells were harvested for RNA isolation for gene expression analysis. Control group: T29-1, T29-2, T80. Testing group: T29A2-8, T29A2-15, T80A2-11.

2010-08-14 | E-GEOD-23599 | biostudies-arrayexpress

The microRNA profile analysis of the function of HMGA2 in immortalized human ovarian surface epithelial cell lines

Project description:To identify HMGA2-regulated downstream target microRNAs, we compared the difference of microRNA profiles between ovarian surface epithelial cells without HMGA2 (T29) and cells with HMGA2 (T29A2). Immortalized ovarian surface epithelial cells (named T29) were transfected with HMGA2 retrovirus vector pBabe-HMGA2 (named T29A2). Then cells were harvested for RNA isolation for microRNA expression analysis.

2010-09-11 | E-GEOD-23634 | biostudies-arrayexpress

The microRNA profile analysis of the function of HMGA2 in immortalized human ovarian surface epithelial cell lines

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Copy number analysis of spontaneously transformed hTERT-immortalized ovarian surface epithelial cells

Project description:We present evidence for cytogenetic changes in two transformed ovarian surface epithelium cell lines, TOSE1 and TOSE4. hTERT-immortalised ovarian surface epithelial cell line spontaneously transformed as measured by growth in soft agar. These cells were grown on plastic, and genomic DNA was extracted and analyzed for cytogenetic changes.

2010-11-19 | GSE25492 | GEO

Copy number analysis of spontaneously transformed hTERT-immortalized ovarian surface epithelial cells

2010-11-19 | E-GEOD-25492 | biostudies-arrayexpress

Comparative transcriptome analysis between immortalized ovarian surface epithelial (iOSE) and immortalized fallopian tube secretory epithelial (iFTE) cells

Project description:The transcriptomes of three immortalized ovarian surface epithelial cell lines (iOSE, PMID: 17266044) and primary OSE cells (Innoprot, Derio, Spain) and four immortalized fallopian tube secretory epithelial (iFTE) cell lines (PMID: 21502498, 22936217) were compared. RNA-sequencing was done from rRNA depleted total RNA (Ribo-Zero rRNA Removal Kit) to approx. 20 million 50 bp paired end reads per sample. A discriminative gene expression signature comprised of 211 genes was developed and used to classify isolated and EpCAM enriched primary ovarian cancer cells (PMID: 25991672). Impact of this signature on overall survival was assessed from several publicly available ovarian cancer gene expression data sets. Background: High grade serous ovarian cancer (HGSOC) is characterized by extensive local, i.e. peritoneal, tumor spread, manifested in two different clinical presentations, miliary (many millet sized peritoneal implants) and non-miliary (few large exophytically growing peritoneal nodes), and an overall unfavorable outcome. HGSOC is thought to arise from fallopian tube secretory epithelial cells, via so called serous tubal intraepithelial carcinomas (STICs) but an ovarian origin was never ruled out for at least some cases. Comparative transcriptome analyses of isolated tumor cells from fresh HGSOC tissues and (immortalized) ovarian surface epithelial and fallopian tube secretory epithelial cell lines revealed a close relation between putative origin and tumor spread characteristic, i.e. miliary from tubes and non-miliary from ovaries.

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Transcription factor HMGA2 controls the K-RAS mediated transformation-specific genetic program

Project description:A genome-wide survey of transcriptional targets responding to chronic KRAS/MAPK (mitogen-activated protein kinase) pathway activation in rat ovarian surface epithelial cells (ROSE 199) has identified multiple differentially expressed transcriptional regulators including the architectural transcription factor high mobility group AT hook 2 (HMGA2). To elucidate the role of HMGA2 in the transcriptional network affected by oncogenic signaling, we used an integrated approach combining RNAi-mediated silencing, microarray-based expression profiling, computational prediction of transcription factor binding sites in target gene promoters and phenotypic analysis. Knocking-down HMGA2 resulted in the reversion of epithelial-mesenchymal transition, loss of anchorage independence and in a substantial restoration of the gene expression pattern characteristic of non-transformed ROSE cells. Computational prediction of transcription factor binding sites in the promoters of HMGA2-regulated genes and expression profiling revealed a preferential role of activator complex-1 (AP-1) components Fra-1 and JunB in target gene regulation. Forced expression of HMGA2 did not transform normal ovarian epithelial cells, suggesting that HMGA2 up-regulation is not sufficient for inducing the transformed phenotype, but mediates cancer-specific phenotypic traits in cells expressing mutated KRAS and, hence, oncogene addiction.

2010-03-01 | GSE14658 | GEO

Expression Data from Ovarian Surface Kinome

2009-04-07 | GSE15578 | GEO

Expression Data from Ovarian Surface Kinome

Project description:The human kinome is incolved in multiple function in the life cycle of cells, and ther differntial expression in cacner suggests that protein kinases play an important role in tumor progression and proliferation. To delineate pathways that may be important for neoplastic change in women at high risk for ovarian cancer, we compared the expression signature of surface kinases in normal ovarian surface epithelium with ovarian epithelium from patients at high risk, and epithelial ovarian cancer using Affymetrix expresion array HG U133Plus2. A total of 18 ovarian samples were collected. The number of samples and subjects for each group were: 5 cancer samples (5 subjects), 6 normal samples (4 patients) and 7 high-risk samples (5 subjects). After the initial inspection, one cancer sample (Sample 9) was excluded from the statistical analysis due to a poor RNA quality.

2009-04-07 | E-GEOD-15578 | biostudies-arrayexpress

Ovarian Cancer gene expression profiling identifies the surface of the ovary as a stem cell niche

Project description:In contrast to epithelial derived carcinomas that arise in most human organs, ovarian surface epithelial cells become more rather than less differentiated as the malignancy progresses. To test the hypothesis that ovarian surface epithelial cells retain properties of relatively uncommitted pluripotent cells until undergoing neoplastic transformation, we conducted gene expression profiling analysis (Affymetrix, U133 Plus 2.0) of 12 ovarian surface epithelial cells and 12 laser capture microdissected serous papillary ovarian cances. We find that over 2000 genes are significantly differentially expressed between the surface epithelial and cancer samples. Network analysis implicates key signaling pathways and pathway interactions in ovarian cancer development. Genes previously associated with adult stem cell maintenance are expressed in ovarian surface epithelial cells and significantly down-regulated in ovarian cancer cells. Our results indicate that the surface of the ovary is an adult stem cell niche and that deregulation of genes involved in maintaining the quiescence of ovarian surface epithelial cells is instrumental in the initiation and development of ovarian cancer.

2009-12-31 | GSE14407 | GEO

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