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Expression data from M0505 (with and without PAX2) murine ovarian surface epithelial cell lines

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE69238 | GEO | 2015/05/27

SECONDARY ACCESSION(S): PRJNA284946

REPOSITORIES: GEO

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Expression data from M0505 (with and without PAX2) 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 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

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.

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

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Genome wide analysis of PAX2 chromatin interaction in MCF-7 cell

Project description:The aim of the study is to understand the role of the transcription factor PAX2 in estrogen receptor positive breast cancer cell line by using ChIP-seq. MCF-7-PAX2 stable cells were cultured in full media and treated with doxycycline (50ng/ml) for 16 hours to induce overexpression of PAX2-HA protein. Then cells were treated with 4-OH-tamoxifen (1μM) for 6 hours. All 3 treatments (Veh, Dox, DoxTam) were performed in duplicates. After treatments, cells were collected for ChIP experiment with HA antibody. ChIP-seq libraries were sequenced and data analysis showed almost no binding in Veh treatment, indicating low backgroud and good quality of the data. PAX transcription factor motif were enriched in PAX2 peaks, indicating the reliability of the data. When crossing the ChIP-seq data with genes regulated by PAX2 in MCF-7, we could observe high level binding of PAX2 to prmoters of PAX2 up-regulated genes and the center of intergenic transcripts induced by PAX2, suggesting the role of PAX2 in regulating transcription activation.

2019-11-08 | GSE140060 | GEO

Pax2 Dependent Expression in the Intermediate Mesoderm at E11.5

Project description:Heterozygous and homozygous Pax2 E11.5 embryos were collected and the intermediate mesoderm was dissected and dispersed into single cells. The Pax2 positive cells also expressed EGFP, which was knocked into the Pax2 locus. EGFP positive cells were sorted by FACS and RNA isolated. We compared RNA expression levels in EGFP positive cells from Pax2 null and Pax2 heterozygote embryos.

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Genome wide analysis of transcripts regulated by PAX2 and Tamoxifen in MCF-7 cells

Project description:The aim of the study is to understand the role of the transcription factor PAX2 in estrogen receptor positive breast cancer cell line by using GRO-seq. MCF-7-PAX2 stable cells were cultured in full media and treated with doxycycline (50ng/ml) for 16 hours to induce overexpression of PAX2. Then cells were treated with 4-OH-tamoxifen (1μM) for 6 hours. All 4 treatments (Veh, Tam, Dox, DoxTam) were performed in duplicates. After treatments, nuclei were isolated and used for nuclear run-on and subsequent GRO-seq library preparation. Libraries were sequenced and data analysis showed that PAX2 could repress estrogen target genes and induce genes enriched in cytokine (TNF-alpha and INF-gamma) related pathways. When combined with tamoxifen, PAX2 could further repress estrogen target genes to a higher degree, and induce genes enriched in p53 related pathway. Moreover, PAX2 could induce the transcription of some intergenic transcripts (potential enhancers) to activate the transcription of nearby genes with could predict good outcome in estrogen receptor positive breast cancer. Overall our finding suggests that PAX2 could benifit ER positive breast cancer by 1) repressing estrogen target genes, and this effect is enhanced by tamoxifen 2) activating cell death/growth arrest related pathways, which is enhanced by potential enhancer transcription induced by PAX2 itself.

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Down-regulation of PAX2 affects ovarian cancer cell growth and migration

Project description:PAX2 is one of nine PAX genes that regulate tissue development and cellular differentiation in embryos. PAX2 promotes cell proliferation, oncogenic transformation, cell lineage specification, migration, and survival. In our previous study, we found that PAX2 is highly expressed in low-grade ovarian serous carcinoma, but its expression in clear cell, endometrioid, and mucinous cell ovarian carcinomas have not been studied. More importantly, the functional role of PAX2 in ovarian cancer is not known. Downregulation of PAX2 in PAX2-expressing ovarian cancer cells inhibits cell proliferation and migration. This growth inhibition is due to the upregulation of the tumor suppressor gene G0S2 and subsequent induction of apoptosis. The PAX2 pathway thus represents a potential therapeutic target for PAX2-expressing ovarian carcinomas. Knockdown PAX2 expression in these cell lines was achieved by lentiviral shRNAs targeting the PAX2 gene. PAX2 stable knockdown cells were characterized for cell proliferation, migration, apoptosis, and gene expression profiles.

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Down-regulation of PAX2 affects ovarian cancer cell growth and migration

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Pax2 Dependent Expression in the Intermediate Mesoderm at E11.5

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Single cell- and Clumps-RNA seq from the trunk of E9.5 Pax2-GFP and Pax2-GFP; Gata3 knockout embryos

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