Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Estrogen regulated microRNAs in mouse ovarian cancer cells.

ABSTRACT: 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.

ORGANISM(S): synthetic construct Mus musculus

PROVIDER: GSE98391 | GEO | 2017/11/30

SECONDARY ACCESSION(S): PRJNA384977

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Both Fallopian Tube and Ovarian Surface Epithelium Can Act as Cell-of-Origin for High Grade Serous Ovarian Carcinoma

Project description:The cell-of-origin of high grade serous ovarian carcinoma (HGSOC) remains controversial, with fallopian tube epithelium (FTE) and ovarian surface epithelium (OSE) both considered candidates. Here, by using genetically engineered mouse models and organoids, we assessed the tumor-forming properties of FTE and OSE harboring the same oncogenic abnormalities. Combined RB family inactivation and Tp53 mutation in Pax8+ FTE caused Serous Tubal Intraepithelial Carcinoma (STIC), which metastasized rapidly to the ovarian surface. These events were recapitulated by orthotopic injection of mutant FTE organoids. Engineering the same genetic lesions into Lgr5+ OSE or OSE-derived organoids also caused metastatic HGSOC, although with longer latency and lower penetrance. FTE- and OSE-derived tumors had distinct transcriptomes, and comparative transcriptomics and genomics suggest that human HGSOC arises from both cell types. Finally, FTE- and OSE-derived organoids exhibited differential chemosensitivity. Our results comport with a dualistic origin for HGSOC and suggest that the cell-of-origin might influence therapeutic response.

2019-10-21 | GSE125016 | GEO

17β-estradiol accelerates ovarian tumour progression in vivo though the upregulation of GREB1

Project description:Exogenous 17β-estradiol (E2) accelerates the progression of ovarian cancer in the transgenic tgCAG-LS-TAg mouse model of the disease. We hypothesized that E2 has direct effects on ovarian cancer cells and this study was designed to determine the molecular mechanisms by which E2 accelerates ovarian tumour progression. Mouse ovarian cancer ascites (MASE2) cell lines were derived from tgCAG-LS-TAg mice. Following intraperitoneal engraftment of MASE2 into SCID mice, exogenous E2 significantly decreased the survival time and increased the tumour burden. Microarray analysis performed on cells derived from mouse ovarian cancer ascites (MASE2) treated with and without E2 indicated that E2 treatment caused the upregulation and downregulation of genes involved in cell differentiation, proliferation and migration. In particular, Greb1 that has been also identified as a hormone-responsive gene in breast cances, was upregulated in mouse tumour cells treated with E2.

2014-01-20 | GSE45271 | GEO

17β-estradiol accelerates ovarian tumour progression in vivo though the upregulation of GREB1

2014-01-20 | E-GEOD-45271 | biostudies-arrayexpress

Global transcriptomic analysis of murine ovarian surface epithelial (MOSE) cells with PAX8 overexpression

Project description:To identify the role of PAX8 in transformation of the ovarian surface epithelium (OSE).

2019-10-01 | GSE128751 | GEO

Transcription profiling of mouse embryonic stem cells reveals novel Disabled-2-associated downstream effectors

Project description:Disabled-2 (DAB2) is up-regulated when ESC were cocultured with OP9 stromal cells for mesodermal colony formation. Expression of DAB2 short hairpin small interfering RNA (shDAB2) altered ESC cell-cell adhesion that subsequently affected colony formation and mesoderm differentiation competence. To further unveil the molecular mechanisms associated with the phenotypic change of shDAB2-expressing ES cells, comprehensive profiling of DAB2-regulated molecules in shDAB2-ES cells (ES-V9 and 285-4) were performed by Affimatrix microarray. Experiment Overall Design: Total RNAs from vector control (ES-V9) and shDAB2-expressing (285-4) ESC were isolated by Trizol (Invitrogen) and were further purified using the RNeasy mini kit (Qiagen). For profiling of mRNA expression, the purified total RNAs were then subjected to microarray analysis (Affymetrix gene chip mouse 430A).

2009-08-23 | E-GEOD-17592 | biostudies-arrayexpress

Transcriptional profile of Epithelial to Mesenchymal Transition in the Ovarian Surface Epithelium

Project description:Adult Ovarian Surface Epithelium (OSE) retains the ability to undergo Epithelial to Mesenchymal Transition (EMT). We established a cell culture of murine adult OSE in their epithelial state, and we induced EMT by modifying their culture conditions. In this experiment we compare the transcriptional profile of the OSE before and after EMT.

2010-01-20 | GSE19947 | GEO

Single cell RNA-seq data for mouse fallopian tube and ovary

Project description:Epithelial ovarian cancer (EOC) is the most lethal malignancy of the female reproductive system. In order to improve EOC patient outcomes, it is crucial to have a better understanding of how EOC develops from its cellular origin. EOCs can originate from either fallopian tube epithelial (FTE) cells or ovarian surface epithelial (OSE) cells, but with different courses of development. The basis for this difference is unclear. To address this, we performed single cell RNA-sequencing of mouse cells isolated from the distal portion of fallopian tubes (i.e., oviducts) and surface layer of ovaries. Analysis of this single cell dataset revealed distinct niche organizations for murine FTE cells and OSE cells.

2022-12-27 | GSE194274 | GEO

Disabled-2 is a negative immune regulator of lipopolysaccharide-stimulated Toll-like receptor 4 internalization and signaling

Project description:Toll-like receptor 4 (TLR4) plays a pivotal role in the host response to lipopolysaccharide (LPS), a major cell wall component of Gram-negative bacteria. Here we elucidated whether the endocytic adaptor protein Disabled-2 (Dab2) that is abundantly expressed in the macrophages plays a role in LPS-stimulated TLR4 signaling and trafficking. Molecular analysis and transcriptome profiling of the RAW264.7 macrophage-like cells expressing short-hairpin RNA of Dab2 revealed that Dab2 mainly regulated LPS-stimulated TRIF-dependent, but not MyD88-dependent TLR4 signaling. Consequently, knockdown of Dab2 augmented TRIF-dependent interferon regulatory factor 3 activation and the expression for the subsets of inflammatory cytokines and interferon-inducible genes. We further delineated that Dab2 acted as a “clathrin sponge” and sequestered clathrin from TLR4/MD2 complex in the resting stage of macrophages. Clathrin was released from Dab2 and associated with TLR4 to facilitate the internalization of TLR4/MD2 complex together with the bound ligand from the cell surface upon LPS stimulation. Dab2 thereby functions as a negative immune regulator of TLR4 endocytosis and signaling, supporting a novel role of Dab2-associated regulatory circuit in the control of inflammatory response of macrophage to endotoxin.

2017-02-09 | GSE81088 | GEO

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

Disabled-2 interacting proteins in U46619-stimulated human platelet activation

Project description:The interacting proteins of Disabled-2 (Dab2) and their functional consequences in U46619-stimulated human platelets were investigated.

2024-10-24 | PXD048490 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data