Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA282460 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The general objective of this study was to investigate the effects of glabridin in Ishikawa cells in comparison to 17β-oestradiol by studying its mechanism of action via Affymetrix GeneChip® PrimeViewTM array The treatments were the unctreated control, 10µM glabridin, 100nM glabridin, 1nM 17β-E2 and the combination treatment of 1nM 17β-E2 with 100nM glabridin. The cells were treated for 72 hours and the RNA were extracted for microarray and RT-qPCR study.
2015-04-29 | E-GEOD-68333 | biostudies-arrayexpress
Project description:The general objective of this study was to investigate the effects of glabridin in Ishikawa cells in comparison to 17β-oestradiol by studying its mechanism of action via Affymetrix GeneChip® PrimeViewTM array
2015-04-29 | GSE68333 | GEO
Project description:Most endometrial cancers are driven by excess estrogen signaling and express the hormone receptor estrogen receptor alpha (ER). Evaluation of the estrogen response in endometrial cancer cells has been limited by the availability of hormonally responsive in vitro models, with one cell line, Ishikawa, being used in most studies. Here, we describe a novel, adherent endometrioid endometrial cancer (EEC) cell line model, HCI-EC-23. We show that HCI-EC-23 retains ER expression and that ER functionally responds to 17b-estradiol (E2) induction over a range of passages. We also demonstrate that this cell line retains paradoxical activation of ER by tamoxifen, which is also observed in Ishikawa and is consistent with clinical data. The mutational landscape shows that HCI-EC-23 is mutated at many of the commonly altered genes in EEC, has relatively few copy-number alterations, and is microsatellite instable high (MSI-high). In vitro proliferation of HCI-EC-23 is modestly enhanced by E2 but is strongly reduced upon combination E2 and progesterone (P4) treatment. HCI-EC-23 exhibit strong E2 dependence for tumor growth in vivo and tumor size is reduced by combination E2 + P4 treatment. Molecular characterization of E2 induction in HCI-EC-23 revealed hundreds of estrogen-responsive genes that significantly overlapped with those regulated in Ishikawa. Analysis of ER genome binding identified similar patterns in HCI-EC-23 and Ishikawa, although ER exhibited more bound sites in Ishikawa. This study demonstrates that HCI-EC-23 is estrogen-responsive and can be used to study the hormonal aspects of endometrial cancer.
2022-08-02 | GSE210122 | GEO
Project description:Most endometrial cancers are driven by excess estrogen signaling and express the hormone receptor estrogen receptor alpha (ER). Evaluation of the estrogen response in endometrial cancer cells has been limited by the availability of hormonally responsive in vitro models, with one cell line, Ishikawa, being used in most studies. Here, we describe a novel, adherent endometrioid endometrial cancer (EEC) cell line model, HCI-EC-23. We show that HCI-EC-23 retains ER expression and that ER functionally responds to 17b-estradiol (E2) induction over a range of passages. We also demonstrate that this cell line retains paradoxical activation of ER by tamoxifen, which is also observed in Ishikawa and is consistent with clinical data. The mutational landscape shows that HCI-EC-23 is mutated at many of the commonly altered genes in EEC, has relatively few copy-number alterations, and is microsatellite instable high (MSI-high). In vitro proliferation of HCI-EC-23 is modestly enhanced by E2 but is strongly reduced upon combination E2 and progesterone (P4) treatment. HCI-EC-23 exhibit strong E2 dependence for tumor growth in vivo and tumor size is reduced by combination E2 + P4 treatment. Molecular characterization of E2 induction in HCI-EC-23 revealed hundreds of estrogen-responsive genes that significantly overlapped with those regulated in Ishikawa. Analysis of ER genome binding identified similar patterns in HCI-EC-23 and Ishikawa, although ER exhibited more bound sites in Ishikawa. This study demonstrates that HCI-EC-23 is estrogen-responsive and can be used to study the hormonal aspects of endometrial cancer.
2022-08-02 | GSE210123 | GEO
Project description:Comparison of gene expression data between wild-type and DM1-affected undifferentiated hES cells.
2025-01-24 | E-GEOD-7179 | ExpressionAtlas
Project description:Expression data from Human Ishikawa cells treated with Genistein
| PRJNA291928 | ENA
Project description:Kynureninase is a member of a large family of catalytically diverse but structurally homologous pyridoxal 5'-phosphate (PLP) dependent enzymes known as the aspartate aminotransferase superfamily or alpha-family. The Homo sapiens and other eukaryotic constitutive kynureninases preferentially catalyze the hydrolytic cleavage of 3-hydroxy-l-kynurenine to produce 3-hydroxyanthranilate and l-alanine, while l-kynurenine is the substrate of many prokaryotic inducible kynureninases. The human enzyme was cloned with an N-terminal hexahistidine tag, expressed, and purified from a bacterial expression system using Ni metal ion affinity chromatography. Kinetic characterization of the recombinant enzyme reveals classic Michaelis-Menten behavior, with a Km of 28.3 +/- 1.9 microM and a specific activity of 1.75 micromol min-1 mg-1 for 3-hydroxy-dl-kynurenine. Crystals of recombinant kynureninase that diffracted to 2.0 A were obtained, and the atomic structure of the PLP-bound holoenzyme was determined by molecular replacement using the Pseudomonas fluorescens kynureninase structure (PDB entry 1qz9) as the phasing model. A structural superposition with the P. fluorescens kynureninase revealed that these two structures resemble the "open" and "closed" conformations of aspartate aminotransferase. The comparison illustrates the dynamic nature of these proteins' small domains and reveals a role for Arg-434 similar to its role in other AAT alpha-family members. Docking of 3-hydroxy-l-kynurenine into the human kynureninase active site suggests that Asn-333 and His-102 are involved in substrate binding and molecular discrimination between inducible and constitutive kynureninase substrates.
| S-EPMC2531291 | biostudies-literature
Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs.
2010-09-25 | GSE24338 | GEO
Project description:RNA extracted at 240min. Samples are rRNA depleted. Expression measurement of Homo sapiens genes.
2019-07-31 | GSE114179 | GEO
Project description:Expression data from human Ishikawa cells treated with Bisphenol A
| PRJNA118613 | ENA