17β-estradiol regulates the release of exosomes via miR-1495p and hnRNPA2/B1 in ER+ breast cancer cells
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ABSTRACT:
ORGANISM(S): synthetic construct Homo sapiens
PROVIDER: GSE127787 | GEO | 2020/03/01
REPOSITORIES: GEO
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Project description:17β-estradiol regulates the release of exosomes via miR-1495p and hnRNPA2/B1 in ER+ breast cancer cells
| PRJNA525398 | ENA
Project description:Assessment of different subcellular localizations (membrane, cytosol, nucleus) of estrogen receptors by multi-epitope protein expression in 200 NSCLC specimens and matched non-cancerous tissues and ESR-1 probe mapping meta-analysis of Affymetrix 2.0 plus data in 1398 NSCLC tumors and normal lung tissues and 39 NSCLC cell lines led us to the conclusion that ERα extranuclear variants are the main ERs in NSCLC. In order to further analyze these effects we treated A549 and H520 cell lines with 17β-estradiol, 17β-estradiol-BSA (plasma membrane impermeable conjugate) and tamoxifen for 3h, in order to investigate early transcriptional effects and responsiveness to estrogen agonists and antagonists. The aim of this study was to demonstrate the functionality of NSCLC ERs and decipher which genes, canonical pathways and networks are affected by each treatment.
2016-12-22 | GSE92679 | GEO
Project description:Transcriptional profiling of zebrafish (Danio rerio) livers comparing control untreated fish with fish treated with estrogen [17β-estradiol (E2)] for different time points (4, 12, 24, 48 hours).
2013-06-28 | GSE45562 | GEO
Project description:Because exosomes have gained attention as a source of biomarkers, we investigated if miRNAs in exosomes (exo-miRs) can report the disease progression of organ injury. Using renal ischemia-reperfusion injury (IRI) as a model of acute kidney injury (AKI), we determined temporally-released exo-miRs in urine during IRI and found that these exo-miRs could reliably mirror the progression of AKI. From the longitudinal measurements of miRNA expression in kidney and urine, we found that release of exo-miRs was regulated sorting process, rather than simply representing their intracellular biosynthesis. In the injury state, miR-16, miR-24, and miR-200c were increased in the urine. Interestingly, expression of target mRNAs of these exo-miRs was significantly altered in renal medulla. Next, in the early recovery state, urinary exo-miRs (miR-9a, miR-141, miR-200a, miR-200c, miR-429), which shares Zeb1/2 as a common target mRNA, were upregulated, indicating that they reflect TGF--associated renal fibrosis. Finally, release of exo-miRs (miR-125a, miR-351) was regulated by TGF-1 and was able to differentiate the sham and IRI even after the injured kidneys were functionally recovered. Altogether, these data indicate that exo-miRs released in renal IRI are largely associated with TGF- signaling. Temporal release of exo-miRs which share targets might be a regulatory mechanism to control the disease progression of AKI.
2019-03-01 | GSE125305 | GEO
Project description:Deep RNA sequceing was performed to explore the expression level of miRNAs in HeLa cell exosomes after treatment with or without 10 ng/ml TGF-β1 for 24 h. The results showed that 48 miRNAs were enriched in exosomes of HeLa cells after treated with TGF-β1 compared with non-treated cells (negative control), proving that TGF-β1 affects HeLa cell exosomes miRNA profile.
2021-02-17 | GSE163507 | GEO
Project description:We hypothesized that miRNAs in the bone maroow mesenchymal stem cells (BM-MSC)-derived exosomes contributed to the phenotype change of breast cancer cells through exosome transfer. We analyzed the miRNA expression signature in BM-MSC-derived exosomes. We compared the miRNA expression levels in exosomes between BM-MSCs and adult fibroblasts (as a control). In this study, miRNA expression including in bone-marrow mesenchymal cell (BM-MSC)-derived exosomes was examined, and compared with that of exosomes derived from adult fibroblast cells or the BM-MSC cells. In addition, miRNA expression of BM-MSC exosomes was also compared with that of breast cancer cells with or without cancer stem cell marker.
2014-07-03 | E-GEOD-58027 | biostudies-arrayexpress
Project description:Bone marrow (BM) niches provide an optimal substrate for multiple myeloma (MM) cell lodgement and growth. Nevertheless, little is known about the putative mechanisms by which the BM microenvironment can lead to initiation or progression of oncogenesis in this disease. We have demonstrated that BM mesenchymal stromal cell-derived exosomes transfer their miRNA and protein content to clonal plasma cells, thus acting as synaptic vesicles responsible for molding the microenvironment surrounding multiple myeloma (MM) cells, leading to MM growth, dissemination and, therefore, disease progression. We used microarray to detail the changes in microRNA expression in MM-BM mesenchymal stromal cell (MSC)-derived exosomes, compared to normal- and monoclonal gammopathy of undetermined significance- BM-MSC-derived exosomes. Exosomes have been isolated from cell culture supernatant of BM-MSCs (MM=7; MGUS=2; Normal=4), and subsequently evaluated at ultrastructural level by using electron microscopy and immunogolf labeling. RNA was extracted; and miRNA profiling has been assessed by using TaqMan human miRNA profiling. Mean miRNA expression value has been used for miRNA RT-qPCR data normalization, as described (Mestdagh et al., 2009).
2013-07-24 | E-GEOD-39571 | biostudies-arrayexpress
Project description:Breast (mammary) cancers in human (BC) and canine (CMT) patients share clinical, pathological, and molecular similarities that suggest dogs may be a useful translational model. Many cancers, including BC, shed exosomes that contain microRNAs (miRs) into the microenvironment and circulation, and these may represent biomarkers of metastasis and tumor phenotype. Three normal canine mammary epithelial cell (CMEC) cultures and 5 CMT cell lines were grown in serum-free media. Exosomes were isolated from culture media by ultracentrifugation then profiled qualitatively. CMEC and CMT cell lines shed round, “cup-shaped” exosomes approximately 150-200 nm by dynamic light scattering (DLS) and immunopositive for exosomal marker CD9 using Western blot. Exosomal small RNA was deep-sequenced on an Illumina HiSeq2500 sequencer and validated by qRT-PCR. Deep-sequencing averaged ~15 million reads/sample. 338 unique miRs were detected, with 145 having > ±1.5-fold difference between one or more CMT and CMEC samples. Gene ontology analysis revealed that the upregulated miRs in this exosomal population regulate a number of relevant oncogenic networks. Several miRNAs including miR-18a, miR-19a and miR-181a were predicted in silico to target the canine estrogen receptor (ESR1α). CMEC and CMT cells shed exosomes in vitro that contain differentially expressed miRs. CMT exosomal RNA expresses a limited number of miRs that are up-regulated relative to CMEC, and these are predicted to target biologically relevant hormone receptors and oncogenic pathways. These results may inform future studies of circulating exosomes and the utility of miRs as biomarkers of breast cancer in women and dogs.
2018-08-13 | GSE116881 | GEO
Project description:17β-HSD1 expression modulates T47D transcript profile in in steroid-deprived medium. The enzyme specifically regulates apoptosis and cancer-related genes in T47D cells cultured in steroid-deprived medium. Genes that primarily involved in Cell cycle progression, such as the Cyclin A2 gene, CCNA2, are generally down-regulated whereas most genes involved in apoptosis and cell death, such as the proapoptotic gene XAF1 and FGF12, are on the contrary up-regulated by 17β-HSD1 knockdown, and 21% of the modulated genes belong to this latter functional category. This correborates with its role previously shown in increasing breast cancer cell proliferation (Aka et al, 2010) and indicates that in addition to its direct role as cell proliferation via incresing E2 and decreasing DHT, 17β-HSD1 may also be involved in oncogenesis by favoring its anti-apoptosis pathway in breast cancer cells 17β-HSD1 may also be involved in oncogenesis by favoring anti-apoptosis pathway and/or inhibiting cell survival pathway. We tested the ability of estrogen to induce or repress endogenous genes of T47D by microarray analysis. A total of 131 genes were found to increase or decrease 1.5-fold or higher in response to 17 beta-estradiol (1 nM for 48 h). Besides, the gene regulation occuring in steroid-deprived conditions showed that 17β-HSD1 modulates gene expression in steroid-independent manners. Our study thus demonstrates that 17β-HSD1 modulates the E2-independent transcription of endogenous genes in T47D cells. The E2-dependent transcription as well as the E2-independent transcription are significantly modulated by 17β-HSD1 in breast cancer cells We first report here that breast cancer cell transcript profile is independtly modulated by both 17β-HSD1 and its principale product estradiol.
2016-09-01 | GSE77345 | GEO
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