RNA-seq of human endometrial cancer cell line Ishikawa treated with BMP2
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB43894 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR5533600_1.fastq.gz | Fastqsanger.gz | |||
| ERR5533600_2.fastq.gz | Fastqsanger.gz | |||
| ERR5533601_1.fastq.gz | Fastqsanger.gz | |||
| ERR5533601_2.fastq.gz | Fastqsanger.gz | |||
| ERR5533602_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 18 |
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Project description:To elucidate the biological function of BMP2 in endometrial cancer cells, Ishikawa, a human endometrial cancer cell line, was stimulated with BMP2 for indicated hours.
2021-09-30 | E-MTAB-10275 | biostudies-arrayexpress
Project description:Our previous studies have shown that bone morphogenetic protein 2 (BMP2), a morphogen belonging to the TGFM-NM-2 superfamily, is markedly induced in human primary endometrial stromal cells (HESC) as they undergo differentiation in response to steroid hormones and cAMP. WNT4 is a downstream target of BMP2 regulation in these cells. To identify the common downstream targets of BMP2 and WNT4 in human endometrial stromal cells, we performed gene expression profling of human ensometrial stromal cell transduced with BMP2 or WNT4 adenovirus. Gene expression profiling revealed that FOXO1, a forkhead family transcription factor and a known regulator of HESC differentiation, is a common downstream mediator of both BMP2 and WNT4 signaling. These studies uncovered a linear pathway involving BMP2, WNT4, and FOXO1 that operates in human endometrium to critically control decidualization. Human endometrial stromal cells were transduced with recombinant adenovirus expressing BMP2, WNT4, or a negative control GFP at MOI 50:1 in 2 ml of culture medium. After transduction for 24 h, the viral particles were removed and the cells were treated with E+P for 3 days to induce decidualization (n=3 for each treatment), pooled total RNA from these cells was then hybridized to high density affymetrix microarrays according to the Affymetrix protocol (Human Genome HG-U133 A2.0 Array) .
2013-02-08 | E-GEOD-39949 | biostudies-arrayexpress
Project description:This group is studying the role of glycoproteins in embryo implantation and development of the maternal-fetal interface. The Aplin lab is developing an embryo implantation model in which blastocysts attach to human endometrial cells. The project aims to investigate the molecular interactions mediating attachment and subsequent events including trophoblast invasion and displacement of maternal cells. In the present phase of the project, the lab is using the Ishikawa (human endometrial) cell line with mouse embryos. RNA from three replicate samples from the Ishikawa cell line were prepared and sent to Microarray Core (E). The RNA was amplified, labeled, and hybridized to the GLYCOv3 microarrays.
2011-04-29 | E-GEOD-28925 | biostudies-arrayexpress
Project description:Our previous studies have shown that bone morphogenetic protein 2 (BMP2), a morphogen belonging to the TGFβ superfamily, is markedly induced in human primary endometrial stromal cells (HESC) as they undergo differentiation in response to steroid hormones and cAMP. WNT4 is a downstream target of BMP2 regulation in these cells. To identify the common downstream targets of BMP2 and WNT4 in human endometrial stromal cells, we performed gene expression profling of human ensometrial stromal cell transduced with BMP2 or WNT4 adenovirus. Gene expression profiling revealed that FOXO1, a forkhead family transcription factor and a known regulator of HESC differentiation, is a common downstream mediator of both BMP2 and WNT4 signaling. These studies uncovered a linear pathway involving BMP2, WNT4, and FOXO1 that operates in human endometrium to critically control decidualization.
2013-02-08 | GSE39949 | 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:This group is studying the role of glycoproteins in embryo implantation and development of the maternal-fetal interface. The Aplin lab is developing an embryo implantation model in which blastocysts attach to human endometrial cells. The project aims to investigate the molecular interactions mediating attachment and subsequent events including trophoblast invasion and displacement of maternal cells. In the present phase of the project, the lab is using the Ishikawa (human endometrial) cell line with mouse embryos.
2011-04-29 | GSE28925 | GEO
Project description:Progestin therapy is one of the preferred treatment modalities for early-stage endometrial cancer patients wishing to retain fertility and for conservatively managing advanced endometrial cancer. However, a significant number of patients currently do not benefit from progestin therapy due to issues such as progestin resistance. In the past, we established a medroxyprogesterone acetate-resistant Ishikawa cell line. From this, we identified the NCF2 gene, which was highly expressed in the resistant group. Functional validation experiments revealed that knocking down NCF2 can effectively reverse progestin resistance. To explore its mechanism, we performed RNA sequencing post-NCF2 knockdown.
2024-06-30 | GSE242226 | GEO
Project description:circRNA-sequencing analysis of Ishikawa human endometrial carcinoma cells treated with MPA or not
| PRJNA748159 | ENA
Project description:In this study the effect of estrogen (E2) and progesterone (P4) and their antagonists Tamoxifen, and Mifepristone (RU486) were assesed in endometrial epithelial cell line Ishikawa and compared to breast cancer cell lines MCF7 and T47D. Concentrations used for E2 and P4 treatments were 10 -8 M and for antagonists 10 -6 M. RNA-Sequencing (Illumina GenomeAnalyzer IIe) was applied to study global gene expression in three different cell lines. Expression values after hormonal or antagonist treatments in two different time points (3h and 12h) were compared to non-treated cells.
2012-01-05 | E-MTAB-822 | biostudies-arrayexpress