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accession-icon SRP076260
Epigenomic remodeling of the PAX8 cistrome in high grade serous ovarian cancer [RNA-Seq]
  • organism-icon Homo sapiens
  • sample-icon 33 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We report mapping of the PAX8 cistrome in three high grade serous ovarian cancer cell lines (KURAMOCHI, OVSAHO, and JHOS4) compared to three benign immortalized fallopian tube cell lines (FT33, FT194, and FT246). We identified a highly conserved PAX8 binding pattern common across benign fallopian tube cell lines that was distinct from the unique PAX8 binding patterns seen in each cancer cell line. Overall design: Comparison of benign and malignant Mullerian cell lines with and without PAX8 knockdown. For each cell line, three distinct siRNAs targeting PAX8 plus a pool of all three siRNAs were examined and compared to both a non-transfected control as well as a control transfected with a non-targeting siRNA.

Publication Title

Epigenetic remodeling regulates transcriptional changes between ovarian cancer and benign precursors.

Sample Metadata Fields

Cell line, Subject

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accession-icon SRP144499
Gene expression analysis of prostate cancer cells treated with fatty acid synthase (FASN) inhibitor IPI-9119
  • organism-icon Homo sapiens
  • sample-icon 22 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Alterations in gene expression following fatty acid synthase inhibtion were evaluated in androgen sensitive LNCaP cells and castration resistant 22Rv1 and LNCaP-95 cells. Cell were exposed to 2 concentrations (0.1 and 0.5 uM) of FASN inhibitor IPI-9119 or DMSO for 6 days. Overall design: Differential gene expression anlaysis in 3 prostate cancer cell lines treated with FASN inhibitor IPI-9119

Publication Title

Inhibition of de novo lipogenesis targets androgen receptor signaling in castration-resistant prostate cancer.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE102964
Novel targets in injured cord in an obese SCI rat model
  • organism-icon Rattus norvegicus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 2.0 ST Array (ragene20st)

Description

In the present study, we sought to understand the impact of obesity/metabolic disease (high-fat induced) on spinal cord injury (SCI) by examining transcriptome. Adult, male Long Evans rats received either thoracic level contusion of the spinal cord or sham laminectomy and then were allowed to recover on normal rat chow for 4 weeks and further on HFD for an additional 8 weeks. Spinal cord tissues harvested from the rats were processed for Affymetrix microarray and further transcriptomic analysis.

Publication Title

Chronic spinal cord changes in a high-fat diet-fed male rat model of thoracic spinal contusion.

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP010291
miR-221 is required for endothelial tip cell behaviors during vascular development
  • organism-icon Danio rerio
  • sample-icon 3 Downloadable Samples
  • Technology Badge IconIlluminaGenomeAnalyzer

Description

Through deep sequencing and functional screening in zebrafish, we find that miR-221 is essential for angiogenesis. miR-221 knockdown phenocopied defects associated with loss of the tip cell-expressed Flt4 receptor. Furthermore, miR-221 was required for tip cell proliferation and migration, as well as tip cell potential in mosaic blood vessels. miR-221 knockdown also prevented “hyper-angiogenesis” defects associated with Notch deficiency and miR-221 expression was inhibited by Notch signaling. Finally, miR-221 promoted tip cell behavior through repression of two targets: cyclin-dependent kinase inhibitor 1b (cdkn1b) and phosphoinositide-3-kinase regulatory subunit 1 (pik3r1). These results identify miR-221 as an important regulatory node through which tip cell migration and proliferation are controlled during angiogenesis. Overall design: Identification of endothelial-expressed microRNA from FACS-isolated zebrafish endothelial cells.

Publication Title

miR-221 is required for endothelial tip cell behaviors during vascular development.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE39402
Gene expression profile of epithelial ovarian tumor tissue of a transgenic mouse model compared to normal mouse ovary tissue
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The etiology of ovarian cancer is poorly understood, mainly due to the lack of an appropriate experimental model for studying the onset and progression of this disease. We have created a mouse model termed ERalpha d/d in which a conditional deletion of estrogen receptor alpha (ERalpha) gene occurred in the anterior pituitary, but ERalpha expression remained intact in the hypothalamus and the ovary. The loss of negative-feedback regulation by estrogen (E) at the level of the pituitary led to elevated production of luteinizing hormone (LH) by this tissue. Hyperstimulation of ovarian cells by LH resulted in increased steroidogenesis, leading to high circulating levels of progesterone, testosterone and E. The ERalpha d/d mice exhibited formation of palpable ovarian epithelial tumors starting at 5 months of age, and by 12 months, most mice carrying these tumors died. Besides proliferating epithelial cells, these tumors also contained an expanded population of stromal cells, which express P450 aromatase suggesting that these cells acquired the ability to synthesize E. In ERalpha d/d mice, in response to the E produced by the stromal cells, the ERalpha signaling is accentuated in the ovarian epithelial cells, triggering increased ERalpha-dependent gene expression, abnormal cell proliferation, and tumorigenesis. The ERalpha d/d animal model of ovarian epithelial tumorigenesis will serve as a powerful tool for exploring the involvement of E-dependent signaling pathways in the etiology of ovarian cancer.

Publication Title

Dysregulated estrogen receptor signaling in the hypothalamic-pituitary-ovarian axis leads to ovarian epithelial tumorigenesis in mice.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE70446
Gene expression profiling of mouse uterine decidua isolated on morning of day 8 of pregnancy
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Placenta development involves complex molecular and cellular interactions between the maternal endometrium and the developing embryo, however, it is not clear what are the precise mechanisms regulating this maternal-fetal crosstalk. Using genetic and cell biological approaches, we have demonstrated that Ras-related C3 botulinum toxin substrate 1 (Rac1), a maternal factor expressed in decidual cells and is markedly elevated in mouse decidua on days 7 and 8 of gestation, regulates the secretory pathways that mediate stromal-endothelial and stromal-trophoblast crosstalk within a narrow temporal window during placenta development.

Publication Title

Rac1 Regulates Endometrial Secretory Function to Control Placental Development.

Sample Metadata Fields

Specimen part

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accession-icon GSE70572
Gene expression profiling of mouse uterus during experimentally induced decidualization
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

To gain insights into the genes whose expression levels are altered during stromal cell differentiation (decidualization), gene microarray profiling was performed following the experimentally induced decidualization protocol.

Publication Title

Rac1 Regulates Endometrial Secretory Function to Control Placental Development.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE146650
Gene expression profiling of mouse uterine stromal cells isolated on day 5 of pregnancy
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Our study revealed that hypoxia inducible factor 2 alpha, Hif2 alpha, is a downstream target of estrogen signaling in mouse uterine stroma at the time of implantation. Further, conditional deletion of Hif2 alpha in mouse uterus leads to infertility due to impaired epithelial remodeling at the time of implantation.

Publication Title

A hypoxia-induced Rab pathway regulates embryo implantation by controlled trafficking of secretory granules.

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE63251
Regulation of LbetaT2 gonadotrope gene expression by GnRH pulses
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

LbetaT2 cells exposed to different number and concentration of GnRH pulses over 4 hours during in vitro perfusion culture

Publication Title

Pulse sensitivity of the luteinizing hormone beta promoter is determined by a negative feedback loop Involving early growth response-1 and Ngfi-A binding protein 1 and 2.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE134890
Pro-BMP9 and pro-BMP10 signalling in pulmonary arterial endothelial cells
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.1 ST Array (hugene21st)

Description

This study was designed to compare the global gene expression change induced by the circulating, prodomain bound forms of BMP9 and BMP10 (pro-BMP9 and pro-BMP10) in human pulmonary arterial endothelial cells (PAECs). This is different from many previous studies which used the growth factor domain of BMP9 and/or BMP10.

Publication Title

Molecular basis of ALK1-mediated signalling by BMP9/BMP10 and their prodomain-bound forms.

Sample Metadata Fields

Sex, Age

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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