Similar Datasets
Project description:To examine the role of Efp in endometrial cancer cells, Ishikawa and HEC-1A cells were treated with siRNA targeting Efp (siEfp) or control siRNA (siControl). Microarray analysis showed that Efp knockdown represses NF-κB-signaling pathway-associated genes.
2018-11-20 | GSE118228 | GEO
Project description:The aim of this study was to establish an in vitro model to investigate the initial stages of human implantation based on co-culture of a) immortalized cells representing the receptive (Ishikawa) or non-receptive (HEC-1-A) endometrial epithelium with b) spheroids of a trophoblastic cell line (JEG-3) modified to express green fluorescent protein. After co-culturing Ishikawa cells with trophoblast spheroids, 310 and 298 genes increased or decreased their expression compared to non-co-cultured Ishikawa control cells, respectively; only 9 genes (5 increased and 4 decreased) were differentially expressed in HEC-1-A upon co-culture with trophoblast spheroids. Compared to HEC-1-A, the trophoblast challenge to Ishikawa cells differentially regulated the expression of 495 genes. In summary, upon co-culture with the trophoblast spheroids, non-receptive epithelium is characterized by a muted transcriptional response which in turn fails to activate the full transcriptional response that trophoblast spheroids undergo when co-cultured with receptive epithelium.
2019-03-14 | GSE121790 | GEO
Project description:Endometrial cancer is the most commonly diagnosed gynecologic malignancy in women after breast, lung and colorectal cancer. Despite numerous scientific advances, the incidence and mortality rate of endometrial cancer is on the rise. Considerable research effort has therefore been placed on understanding the pathogenesis of this disease to combat this growing issue. There is now emerging evidence to suggest a putative role for dysregulation of the renin angiotensin system (RAS) and in particular the (pro)renin receptor ((P)RR), in the ontogenesis of endometrial cancer. Support for this notion arises from previous literature implicating (P)RR in cancer pathophysiology (e.g., breast cancer and pancreatic carcinoma) by virtue of its role in proliferation, angiogenesis, fibrosis, migration and invasion. In view of these data, we aimed to investigate the functional role of (P)RR in human endometrial cancer progression and development. To this end, we employed an siRNA-mediated knock down approach to abrogate (P)RR expression in the immortalized endometrial epithelial cell lines; Ishikawa, AN3CA and HEC-1A to explore the role of (P)RR in cellular proliferation and cellular viability. To further extend these analyses we also carried out a sophisticated proteomic screen, that investigated the potential pathways via which (P)RR is acting in endometrial cancer physiology. These data confirmed that (P)RR is critical for endometrial cell cancer development, contributing to both its proliferative capacity and in the maintenance cell viability. This is likely mediated through proteins such as MGA, SLC4A7, SLC7A11 or DHRS2, which were reduced following (P)RR knockdown. These putative protein interactions/pathways, which rely on the presence of (P)RR, are likely to contribute to endometrial cancer progression and could therefore, represent several novel therapeutic targets in the treatment of this cancer. Finally we contend that (P)RR, in its soluble form (s(P)RR) in blood, may have substantial potential as a novel biomarker for cancer diagnosis and prognosis prediction going forward.
2022-04-23 | PXD023042 | Pride
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: Not available
| S-EPMC4453454 | biostudies-literature
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:The goal of this study is to compare transcriptome profiling of SF3B1 depleted Ishikawa endometrial cancer cells by RNA-sequencing Methods: SF3B1 depleted mRNA profiles of control siRNA treated and SF3B1 siRNA treated Ishikawa endometrial cancer cells were generated by deep sequencing, in triplicate using Illumina HiSeq 3000 sequencers with 2×150 paired-end reads. Basecalls and demultiplexing were performed with Illumina’s RTA version 1.9 and bcl2fastq2 software with a maximum of one mismatch in the indexing read. RNA-seq reads were then aligned to the Ensembl release 76 primary assembly with STAR version 2.0.4b. qRT–PCR validation was performed using TaqMan assays Results: Using a 2.5-fold cutoff and Benjamini-Hochberg false discovery rate (FDR) of <0.01 threshold for inclusion, we identified 1,992 differentially expressed genes (DEGs) between Control and SF3B1 depleted Ishikawa cells Conclusions: Our study represents the first detailed analysis of SF3B1 depleted Ishikawa endometrial cancer cells transcriptomes, with biologic replicates, generated by RNA-seq technology.
2020-12-30 | GSE156775 | GEO
Project description:Using H3K27ac ChIP-seq profile to map active enhancers in lung cancer and endometrial carcinoma cells ChIP-seq of H3K27ac was done in lung adenocarcinoma cell lines (NCI-H358 and NCI-H2009), squamous cell lung carcinoma cell lines (HCC95) and endometrial carcinoma cell lines (Ishikawa)
2015-10-26 | E-GEOD-66992 | biostudies-arrayexpress
Project description:Endometrial receptivity is defined as the functional, morphological, and molecular changes of the endometrium occurring during a limited time period in the menstrual cycle called the ‘window of implantation’. The endometrial luminal epithelial cells are critical in producing this receptivity as their adhesive capacity enables embryo implantation; however, how this occurs is poorly understood. Recently, using endometrial epithelial organoids, we identified that Myosin Heavy Chain 10 (MYH10) was abnormally downregulated in infertile endometrial epithelial cells during the window of implantation, suggesting a role in receptivity. MYH10 regulates processes important in endometrial receptivity including cell polarity, adhesion, and migration; however, whether it regulates endometrial receptivity has yet to be researched. We aimed to investigate whether MYH10 regulates endometrial epithelial cell adhesive capacity. MYH10 localised to all major cellular compartments within endometrial tissue. However, immunostaining intensity was higher in luminal epithelial cells during the window of implantation compared to the proliferative phase in fertile endometrium. Conversely, this increased expression was not maintained in infertile endometrium during the window of implantation. siRNA knockdown of MYH10 in the receptive Ishikawa cell line significantly decreased cell adhesion to human cytotrophoblast-progenitor spheroids. MYH10 knockdown in Ishikawa cells also increased PGR, FOXO1, and GPX3 expression, while decreasing PDLIM2 expression. Proteomics analysis following MYH10 knockdown altered the production of 57 proteins with functions critical in endometrial receptivity including tight junction regulators. These results demonstrate that MYH10 alters endometrial epithelial cell adhesive capacity primarily via regulation of the actin cytoskeleton, implying an important role in implantation.
2026-05-05 | PXD062326 | Pride
Project description:The role of obesity in endometrial cancer development is tested by co-culturing adipose stromal cells (ASCs) with endometrial epithelial cells and endometrial cancer cell Ishikawa for 21 days. Control cells (not exposed to ASCs) were incubated for the same duration. RNA-seq identified differential expression due to ASC exposure
2019-02-13 | GSE103203 | GEO