Further, top three core targets of FN anti-OGS were determined as oestrogen receptor 1 (ESR1), tumour protein p53 (TP53), receptor tyrosine-protein kinase erbB-2 (ERBB2) respectively.
In human data, OGS samples showed increased expressions of ERα, p-PI3KCA<sup>Tyr317</sup> , and p-AKT <sup>Ser473</sup> proteins, followed by notably upregulated miR-375 content in comparison with that in OGS-free.
Overall, the COS grafted estrogen-functionalized cationic liposomes, fortified with glutathione-responsiveness, showed great potential for specific intracellular drug delivery to estrogen receptor-expressing tumors such as osteosarcoma.
The aim of this study was to investigate the effects of calycosin on apoptosis of estrogen receptor (ER)-positive and ER-negative human osteosarcoma cell lines and tumor xenografts in mice.
Overlaps between DEGs and ESR1 target genes which contained peaks in promoters were considered as reliable E2-mediated genes through ESR1 in osteosarcoma.
Tumor protein p53 (TP53), mitogen-activated protein kinase 1 (MAPK1) and estrogen receptor 1 (ESR1) were identified the most important osteosarcoma‑associated genes, with the highest levels of topological properties.
In this study, OS cell MG-63 was treated with low (1 nM) or high (100 nM) dose of 17β-Estradiol (E2) with the presence or absence of estrogen receptor α (ERα), for evaluating the E2 effects on proliferation, migration, invasion, colony formation and apoptosis.
First we focused on their estrogen receptor alpha and beta (ERalpha and ERbeta) selectivity, second we addressed structure-activity relationships, using bone-derived human osteosarcoma cell line (U2OS cells) stably expressing ERalpha or transiently expressing ERbeta.
Estrogen receptor alpha and beta heterodimers exert unique effects on estrogen- and tamoxifen-dependent gene expression in human U2OS osteosarcoma cells.
Transcriptional profiling of estrogen-regulated gene expression via estrogen receptor (ER) alpha or ERbeta in human osteosarcoma cells: distinct and common target genes for these receptors.
For the molecular analysis, genetic polymorphisms of the VDR (Fok I, Apa I, and TaqI), ER (Pvu II and XbaI), and COLIalpha1 (Msc I) genes were characterized in 72 osteosarcoma and 53 Ewing sarcomas and in a group of 143 healthy matched children.
Using human estrogen receptor (ER) as a model nuclear receptor, we demonstrate how this approach can be successfully applied to assay development in Saos-2 human osteosarcoma cells.
Furthermore, 2-ME was similarly effective at killing immortalized human fetal osteoblastic cells (hFOB) with and without estrogen receptor-alpha and -beta and rat osteosarcoma cells (ROS17/2.8).
To study the mechanism of ER in regard to E2-mediated effects, we stably transfected a human osteosarcoma cell line, SaOS-2, with an expression vector, pMV-7-ER, containing the human ER gene.
RNA blot analysis with a complementary DNA probe to the human estrogen receptor revealed putative receptor transcripts of 6 to 6.2 kilobases in both rat and human osteosarcoma cells.