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Establish the mechanism of the effect of panobinostat on murine Pax2+ renal progenitors.

ABSTRACT: Establish the mechanism of the effect of panobinostat on murine Pax2+ renal progenitors.

PROVIDER: PRJNA802179 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17833800_1.fastq.gz	Fastqsanger.gz
	SRR17833800_2.fastq.gz	Fastqsanger.gz
	SRR17833769_1.fastq.gz	Fastqsanger.gz
	SRR17833769_2.fastq.gz	Fastqsanger.gz
	SRR17833770_1.fastq.gz	Fastqsanger.gz

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Establish the mechanism of the effect of panobinostat on murine Pax2+ renal progenitors.

Project description:We generated single-cell RNA sequencing (scRNAseq) datasets of primary cultures of mouse Pax2+ renal progenitors isolated from healthy mice and treated in vitro with vehicle or the HDAC inhibitor panobinostat. Pax2+ cells expressed progenitor cells markers in absence of tubular and endothelial cell markers and following treatment with panobinostat, upregulated the expression of podocyte-specific markers.

2022-09-23 | GSE195785 | GEO

Differential gene expression in neuroblastoma cells after treatment with vehicle control, JQ1, panobinostat, or combination of JQ1 and panobinostat

Project description:The bromodomain inhibitor JQ1 and the histone deacetylase inhibitor panobinostat induce synergistic anticancer effects We analyzed whether JQ1 and panobinostat synergistically modulate gene expression Neuroblastoma SK-N-BE(2) cells were treated with vehicle control, 1 microM JQ1, 10 nM panobinostat, or combination of JQ1 and panobinostat for 6 hours, and subjected to differential gene expression studies with Affymetrix microarrays.

2015-12-31 | E-GEOD-68690 | biostudies-arrayexpress

PAX2-null progenitors define multiple lineages with common expression signatures in benign and neoplastic oviductal epithelium

Project description:The oviducts contain high grade serous cancer precursors, which are M-NM-3-H2AXp and p53 mutation positive. Secretory cell outgrowths (SCOUTs) are associated with older age and serous cancer. We evaluated PAX2 expression in proliferating oviductal cells, normal mucosa, SCOUTs, Walthard cell nests, STINs and HGSCs. Non-ciliated cells in normal mucosa were PAX2 positive but became PAX2 negative in multilayered epithelium. PAX2 negative SCOUTs fell into two groups; Type I were secretory or secretory/ciliated with a M-bM-^@M-^\tubalM-bM-^@M-^] phenotype and were ALDH1 negative. Type II displayed a columnar to pseudostratified phenotype, with an EZH2,ALDH1, M-NM-2-catenin, Stathmin, LEF1, RCN1 and RUNX2 expression signature . This study, for the first time, links PAX2 negative with proliferating fetal and adult oviductal cells undergoing basal and ciliated differentiation and shows that this expression state is maintained in SCOUTs, STINs and HGSCs. All three entities can demonstrate a consistent perturbation of genes involved in potential tumor suppressor gene silencing (EZH2), transcriptional regulation (LEF1), regulation of differentiation (RUNX2) calcium binding (RCN1) and oncogenesis (Stathmin). This shared expression signature between benign and neoplastic entities links normal progenitor cell expansion to abnormal and neoplastic outgrowth in the oviduct and exposes a common pathway that could be a target of early prevention. 17 total samples are analyzed. 4 for TYPE 1 SCOUTs, 3 for TYPE 2 SCOUTs, 7 for paired normal epithelium, 3 for tumor

2014-09-20 | E-GEOD-58842 | biostudies-arrayexpress

PAX2-null progenitors define multiple lineages with common expression signatures in benign and neoplastic oviductal epithelium

Project description:The oviducts contain high grade serous cancer precursors, which are γ-H2AXp and p53 mutation positive. Secretory cell outgrowths (SCOUTs) are associated with older age and serous cancer. We evaluated PAX2 expression in proliferating oviductal cells, normal mucosa, SCOUTs, Walthard cell nests, STINs and HGSCs. Non-ciliated cells in normal mucosa were PAX2 positive but became PAX2 negative in multilayered epithelium. PAX2 negative SCOUTs fell into two groups; Type I were secretory or secretory/ciliated with a “tubal” phenotype and were ALDH1 negative. Type II displayed a columnar to pseudostratified phenotype, with an EZH2,ALDH1, β-catenin, Stathmin, LEF1, RCN1 and RUNX2 expression signature . This study, for the first time, links PAX2 negative with proliferating fetal and adult oviductal cells undergoing basal and ciliated differentiation and shows that this expression state is maintained in SCOUTs, STINs and HGSCs. All three entities can demonstrate a consistent perturbation of genes involved in potential tumor suppressor gene silencing (EZH2), transcriptional regulation (LEF1), regulation of differentiation (RUNX2) calcium binding (RCN1) and oncogenesis (Stathmin). This shared expression signature between benign and neoplastic entities links normal progenitor cell expansion to abnormal and neoplastic outgrowth in the oviduct and exposes a common pathway that could be a target of early prevention.

2014-09-20 | GSE58842 | GEO

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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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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.

2011-12-05 | E-GEOD-30501 | biostudies-arrayexpress

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

2011-12-05 | GSE30501 | GEO

Pax2 Dependent Expression in the Intermediate Mesoderm at E11.5

2014-12-13 | GSE64129 | GEO

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

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

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2021-02-16 | GSE143806 | GEO

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