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Changes in follistatin levels by BRCA1 may serve as a regulator of ovarian carcinogenesis

ABSTRACT: Follistatin is a folliculogenesis regulating protein that has been found in relatively high concentration in the female ovarian tissues. Follistatin acts as an antagonist to the function of Activin, which is often found elevated in ovarian carcinogenesis and thus presents a possibility for therapeutic intervention in controlling ovarian cancer. Most of the ovarian cancer occurs in its ovarian surface epithelium (OSE) cells. Although breast cancer susceptibility gene 1 (BRCA1) is a known tumor suppressor for breast cancer but its role in ovarian cancer is beginning to unfold. We have shown that in ovarian carcinoma cells (SKOV3), stable overexpression of BRCA1 stimulates Follistatin secretion and simultaneously downregulates Activin expression. Moreover, knock down of BRCA1 in immortalized OSE (IOSE) cells from human ovarian tissue demonstrates downregulation of Follistatin secretion with simultaneous up regulation of Activin expression. IOSE cells generated from an ovarian cancer patient with BRCA1 mutation failed to secrete Follistatin in the medium. Our results indicate a novel function for BRCA1 in the form of regulation of the expression of Follistatin in the ovarian cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE30296 | GEO | 2011/07/02

SECONDARY ACCESSION(S): PRJNA143795

REPOSITORIES: GEO

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Changes in follistatin levels by BRCA1 may serve as a regulator of ovarian carcinogenesis

Project description:Follistatin is a folliculogenesis regulating protein that has been found in relatively high concentration in the female ovarian tissues. Follistatin acts as an antagonist to the function of Activin, which is often found elevated in ovarian carcinogenesis and thus presents a possibility for therapeutic intervention in controlling ovarian cancer. Most of the ovarian cancer occurs in its ovarian surface epithelium (OSE) cells. Although breast cancer susceptibility gene 1 (BRCA1) is a known tumor suppressor for breast cancer but its role in ovarian cancer is beginning to unfold. We have shown that in ovarian carcinoma cells (SKOV3), stable overexpression of BRCA1 stimulates Follistatin secretion and simultaneously downregulates Activin expression. Moreover, knock down of BRCA1 in immortalized OSE (IOSE) cells from human ovarian tissue demonstrates downregulation of Follistatin secretion with simultaneous up regulation of Activin expression. IOSE cells generated from an ovarian cancer patient with BRCA1 mutation failed to secrete Follistatin in the medium. Our results indicate a novel function for BRCA1 in the form of regulation of the expression of Follistatin in the ovarian cells. 3 treatments vs 3 controls

2011-07-02 | E-GEOD-30296 | biostudies-arrayexpress

Transcription profiling of human IOSE cells treated with TGFb1, time series

Project description:Unlike ovarian cancer, normal ovarian epithelium response to TGFb1 induced growth inhibition. This time course study tried to idenify genes that showed changes after additionof TGFb1 in immortalized ovarian surface epithelial cells (IOSE) which is derived from normal ovarian epithelial cells Experiment Overall Design: IOSE cells were treated with TGFb1 for 0, 3, 6, and 12hrs. Cells were harvested for total RNA extraction. Affymetrix expression microarray was performed to analyse gene expression changes.

2008-06-15 | E-GEOD-6653 | biostudies-arrayexpress

TGFb/Smad4 targets promter in IOSE cells

Project description:Unlike ovarian cancer, normal ovarian epithelium response to TGFb1 induced growth inhibition. This study tried to idenify promoters that showed Smad4 binding after additionof TGFb1 in immortalized ovarian surface epithelial cells (IOSE) which is derived from normal ovarian epithelial cells Keywords: ChIP-chip

2007-01-13 | GSE6727 | GEO

Gene expression analysis of IOSE cells treated with TGFb1, a time course study

2007-01-09 | GSE6653 | GEO

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.

2016-12-15 | E-MTAB-5240 | biostudies-arrayexpress

Global Profiling of Activin Target Genes in Mouse Granulosa Cells

Project description:In order to understand the mechanisms and pathways by which activin regulates follicle function, we performed a microarray study and identified activin regulated genes in mouse ovarian granulose cells. Primary cultured ovarian granulosa cells collected from day 21-23 old immature mice were treated with Activin A (A), Activin A plus its antagonist follistatin (AplusF), and PBS (P, vehicle) for 24 h. RNA from each treatment group was isolated and the experiments were repeated four times. Samples from experiment one were assigned as P1, A1 and A+F1, samples from experiment two as P2, A2 and A+F2, and so on. About 100 ng of each RNA sample was amplified using a modified Eberwine T7-based amplification protocol and hybridized to the Illumina Sentrix Mouse-6 Expression BeadChip (Illumina, Inc., San Diego, CA) that contains 48,000 sets of oligonucleotides.

2011-03-02 | E-GEOD-20583 | biostudies-arrayexpress

Proteomics of Primary cells derived from Ovarian Cancer

Project description:We analyzed primary cells derived from patients with ovarian cancer. We compared OSE, FTE and EOC and we use quantitative propeomics followed by WB, IHC, TMA for validation of our findings. We also analyzed the phosphoproteome of OVCAR3.

2017-04-03 | PXD003531 | Pride

Expression data from M0505 and STOSE murine ovarian surface epithelial cell lines

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 spontaneously transformed into the spontaneously transformed OSE (STOSE) cell line in mid 2012. We used microarrays to try to determine the molecular pathways that may have lead to the transformation of M0505 cells into STOSE cells to gain information that may lead to a greater understanding of human ovarian cancer initiation.

2014-02-04 | GSE54633 | GEO

Molecular Profiling provides evidence of the existence of two functionally distinct classes of ovarian cancer stroma

Project description:RNA microarray profiling of 45 tissue samples was carried out using the Affymetrix (U133) gene expression platform. Laser capture microdissection (LCM) was employed to isolate cancer cells from the tumors of 18 serous ovarian cancer patients (Cepi). For 7 of these patients, a matched set of surrounding cancer stroma (CS) was also collected. For controls, surface ovarian epithelial cells (OSE) were isolated from the normal (non-cancerous) ovaries of 12 individuals including matched sets of samples of OSE and normal stroma (NS) from 8 of these patients. Unsupervised hierarchical clustering of the microarray data resulted in the expected separation between the OSE and Cepi samples. Consistent with models of stromal activation, we also observed significant separation between the NS and CS samples. Unexpectedly, the CS samples sub-divided into two distinct groups. Analysis of expression patterns of genes encoding signaling molecules and compatible receptors in the CS and Cepi samples are consistent with the hypothesis that the two CS sub-groups differ significantly in their relative propensities to support tumor growth.The results indicate the existence of distinct categories of ovarian cancer stroma and suggest that functionally significant variability exists among ovarian cancer patients in the ability of the microenvironment to modulate cancer development. Gene expression analysis of 8 normal stroma (NS) and 8 matched normal ovarian surface epithelium (OSE) from 12 individuals, along with 7 cancer stroma and 7 matched cancer epithelium from 18 additional ovarian cancer patients

2012-06-13 | E-GEOD-38666 | biostudies-arrayexpress

Estrogen regulated microRNAs in mouse ovarian cancer cells.

Project description:In a mouse model of ovarian cancer, we have established that prolonged exposure to 17β-estradiol (E2) accelerates tumour onset and increases the incidence of morphologically dysplastic ovarian surface epithelium (OSE). OSE cell proliferation and morphology are tightly regulated by the asymmetrical distribution of polarity proteins that provide positional cues for surface localization and growth inhibition. We hypothesized that E2 causes OSE dysplasia by inhibiting a tumour suppressor gene called Disabled-2 (Dab2). Dab2 is critical in mediating the polarized distribution of cell surface proteins and is highly expressed in normal OSE, but is absent in the majority of ovarian cancers. In this study, Dab2 is shown to be suppressed by E2 and we investigated the possibility that this occurs through E2 up-regulation of microRNAs. microRNA microarray analysis comparing control vs. E2 treated mouse ovarian cancer cells (MASE) was used to identify candidate miRNAs that have a seeding sequence capable of targeting the 3-prime untranslated region (3’UTR) of both human and mouse Dab2 transcript.

2017-11-30 | GSE98391 | GEO

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