Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA128849 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:MicroRNAs (miRNAs) in body fluids are candidate diagnostics for a variety of conditions and diseases, including breast cancer. One premise for using extracellular miRNAs to diagnose disease is the notion that the abundance of the miRNAs in body fluids reflects their abundance in the abnormal cells causing the disease. As a result, the search for such diagnostics in body fluids has focused on miRNAs that are abundant in the cells of origin. Here we report that released miRNAs do not necessarily reflect the abundance of miRNA in the cell of origin. We find that release of miRNAs from cells into blood, milk and ductal fluids is selective and that the selection of released miRNAs may correlate with malignancy. In particular, the bulk of miR-451 and miR-1246 produced by malignant mammary epithelial cells was released, but the majority of these miRNAs produced by non-malignant mammary epithelial cells was retained. Our findings suggest the existence of a cellular selection mechanism for miRNA release and indicate that the extracellular and cellular miRNA profiles differ. This selective release of miRNAs is an important consideration for the identification of circulating miRNAs as biomarkers of disease.
2010-09-10 | GSE22235 | GEO
Project description:MicroRNAs (miRNAs) in body fluids are candidate diagnostics for a variety of conditions and diseases, including breast cancer. One premise for using extracellular miRNAs to diagnose disease is the notion that the abundance of the miRNAs in body fluids reflects their abundance in the abnormal cells causing the disease. As a result, the search for such diagnostics in body fluids has focused on miRNAs that are abundant in the cells of origin. Here we report that released miRNAs do not necessarily reflect the abundance of miRNA in the cell of origin. We find that release of miRNAs from cells into blood, milk and ductal fluids is selective and that the selection of released miRNAs may correlate with malignancy. In particular, the bulk of miR-451 and miR-1246 produced by malignant mammary epithelial cells was released, but the majority of these miRNAs produced by non-malignant mammary epithelial cells was retained. Our findings suggest the existence of a cellular selection mechanism for miRNA release and indicate that the extracellular and cellular miRNA profiles differ. This selective release of miRNAs is an important consideration for the identification of circulating miRNAs as biomarkers of disease. miRNA microarrays were screened by LC Sciences. One microgram of MCF7 cellular RNA preparation was labeled with Cy3, and one microgram of the extracellular RNA samples was labeled with Cy5. In brief, the RNA was labeled with Cy5 or Cy3 and hybridized to LCSciences standard arrays for mature miRNA of all species available in the Sanger miRBase database (Release 12.0). The data were analyzed including background subtraction, using a LOWESS (locally weighted regression) method on the background-subtracted data. Only transcripts with a signal intensity higher than 3X (background SD) and spot CV<0.5. CV was calculated by (SD)/(signal intensity), and in which repeating probes on the array produced signals from at least 50% of the repeating probes are above detection level.
2010-09-10 | E-GEOD-22235 | biostudies-arrayexpress
Project description:SAGE analysis of normal human mammary epithelial cells, breast carcinoma (malignant effusion), and breast adenocarcinoma (malignant pleural effusion)
| PRJNA134105 | ENA
Project description:The crosstalk between tumor cells and the adjacent normal epithelium contributes to cancer progression, but its regulators have remained elusive. Here, we show that breast cancer cells maintained in hypoxia release small extracellular vesicles (sEV) that activate mitochondrial dynamics, stimulate mitochondrial movements and promote organelle accumulation at the cortical cytoskeleton in normal mammary epithelial cells. This results in Akt activation, membrane focal adhesion turnover and increased epithelial cell migration. RNA-Seq profiling identified Integrin-Linked Kinase (ILK) as the most upregulated pathway in sEV-treated epithelial cells and genetic or pharmacologic targeting of ILK reversed mitochondrial reprogramming and suppressed sEV-induced cell movements. In a three-dimensional model of mammary gland morphogenesis, sEV treatment induced hallmarks of malignant transformation, with deregulated cell death/cell proliferation, loss of apical-basal polarity and appearance of epithelial-to-mesenchymal transition (EMT) markers. Therefore, sEV released by hypoxic breast cancer cells reprogram mitochondrial dynamics and induce oncogenic changes in a normal mammary epithelium
2020-11-12 | GSE154340 | GEO
Project description:miRNA expression data from normal and Malignant hematopoietic cells
| PRJNA225798 | ENA
Project description:Columnar cell hyperplasia (CCH) is the first histologically identifiable lesion in the breast with premalignant potential. Altered miRNA expression in the stroma surrounding CCH compared to normal tissue was discovered. The effect of upregulation of one specific miRNA was investigated by gene expression array in human mammary fibroblasts as well as in epithelial CCH cells coculterd with miR-132 oversexpressing human mammary fibroblasts. We used microarrays to detail the effects of miR-132 in human mammary fibroblasts and identified multiple altered genes and gene pathways both in the fibroblasts and in cocultured human mammary epithelial CCH cells.
2014-07-15 | GSE46197 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE32727: EMT inducers catalyze malignant transformation of mammary epithelial cells and drive tumorigenesis towards claudin-low tumors [human] GSE32904: EMT inducers catalyze malignant transformation of mammary epithelial cells and drive tumorigenesis towards claudin-low tumors [mouse] Refer to individual Series
2012-07-23 | E-GEOD-32905 | biostudies-arrayexpress
Project description:Preclinical and clinical studies have shown for decades that tumor cells demonstrate significantly enhanced sensitivity to “fever range” hyperthermia (increasing the intratumoral temperature to 42-45oC) than normal cells, although it is unknown why cancer cells exhibit this distinctive susceptibility. To address this issue, mammary epithelial cells and three malignant breast cancer lines were subjected to hyperthermic shock and microarray analysis of the global transcription changes was subsequently performed. MCF10A (mammary epithelial cells) and MCF7, MDA231, and MDA468 breast cancer cells were grow at normal growth temperatures or subjected to 30 minutes of hyperthermic (45oC) shock followed by replacement with conditioned media at normal growth temperatures. RNA was collected 4 hours after shock and subjected to microarray analysis.
2013-12-01 | E-GEOD-48398 | biostudies-arrayexpress
Project description:The distinct frequency of activation of the RAS/MAPK signaling pathway in human cancers suggests a context-dependent cellular state of vulnerability to RAS transformation. While uncommon in breast cancers, oncogenic activation of this pathway is frequent in claudin-low (CL) tumors, a subtype of breast malignancies enriched in features of epithelial-mesenchymal transition (EMT), suggesting an interplay between RAS activation and EMT. Using inducible models of human mammary epithelial cells, we show that RAS-mediated transformation relies upon cellular reprogramming governed by the EMT-inducing transcription factor ZEB1. The path to ZEB1 induction involves a paracrine process: cells entering a senescent state following RAS induction release proinflammatory cytokines, notably IL-6 and IL1 which promote ZEB1 expression and activity in neighboring cells, thereby fostering their malignant transformation. Collectively, our findings unveil a previously unprecedented role for senescence in bridging RAS activation and EMT over the course of malignant transformation of human mammary epithelial cells.
2024-02-16 | GSE201536 | GEO