Similar Datasets
Project description:We report that EVs originated from cancer cells can modulate glucose metabolism in the recipient cancer cells and induce cell proliferation and aggressive phenotype. Two breast cancer cell lines with different levels of glycolytic activity, MDA-MB-231 of a claudin low-type breast cancer cell and MCF7 of luminal type breast cancer cell, were selected and co-cultured, as the originating and recipient cells using indirect co-culture system such as transwell system or microfluidic system. Proteomic profiling of the co-cultured MCF7 cells revealed proliferation and dedifferentiation of the MCF7 cells following co-culture with the MDA-MB-231 cells. Transcriptomic analysis demonstrated that glycolysis increased in the co-cultured MCF7 cells, and the component analysis of glycolysis-related genes revealed that the second-most component after cytoplasm was extracellular exosomes. In addition, 36 significant KEGG pathways were identified in a total of 856 proteins identified by proteomin analysis of MDA-MB-231-induced EVs. Among these pathways were the main pathways (glycolysis/gluconeogenesis, pyruvate metabolism, and PI3K-Akt signaling pathways) that could explain the metabolic modulation of MCF7 cells. In our work, we indirectly show that it is MDA-MB-231-derived EVs that play an important role in this phenomenon. Our study highlights the potential effects of aggressive cancer cells on other surrounding cancer cells through EVs.
2021-09-09 | GSE183551 | GEO
Project description:Full title: Expression data from antisense miRNA-221/222 (si221/222) and control inhibitor (GFP) treated fulvestrant-resistant breast cancer cells The expression of miR-221/222 were found to be upregulated in fulvestrant resistant breast cancer cells MCF7-FR compared to its drug-sensitive counterpart MCF7. To investigate the role of miR-221/222 in acquired resistance to fulvestrant, we lowered the level of miR-221/222 in MCF7-FR cells using miRNA inhibitors (antagomirs), and compared gene expression profiles before and after treatment. Fulvestrant-resistant breast cancer cells MCF7-FR (originated from drug-sentitive breast cancer model cell line MCF7) were transient-transfected by antigomirs targeting miR221 or miR222 (i.e. si221, si222). All three cell lines, MCF7-FR, siR221, siRNA222 were subjected to gene expression profiling.
2011-01-29 | E-GEOD-19777 | biostudies-arrayexpress
Project description:The effect of Eribulin in RNA expression was addressed by RNA-sequence using Eribulin treated MCF7 breast cancer cell line.
2023-12-27 | GSE226836 | GEO
Project description:Desmocollin-1 (DSC1) is a desmosomal transmembrane glycoprotein that maintains cell-to-cell adhesion. DSC1 was previously associated with lymph node metastasis of luminal A breast tumors and was found to increase metastatic potential of MCF7 cells in vitro. To delineate DSC1 role in breast cancer metastasis and evaluate possibilities of DSC1 modulation, we investigated the effect of DSC1 overexpression on morphology, cell survival, transcriptome, proteome and interactome of MCF7 cells, a luminal A breast cancer model, stably transduced with lentiviral vector carrying DSC1 gene (MCF7-DSC1-GFP). We moreover identified inhibitor parthenolide to decrease DSC1 protein levels and to modulate the molecular mechanisms associated with DSC1 in MCF7 cells. This PRIDE project includes quantitative analysis results for the total proteome LC-DIA-MS/MS experiment evaluating DSC1 overexpression and parthenolide treatment in MCF7 breast cancer cell line, and results of pulldown analysis of DSC1-interacting proteins in MCF7 cells with and without parthenolide treatment.
2023-10-24 | PXD041029 | Pride
Project description:From the parental breast cancer cell line MCF7 (weakly invasive), we progressively selected hyperinvasive subclones. We compared the gene expression between the parental MCF7-I0 and the hyper-invasive cells MCF7-I6. We used Affymetrix U133 Plus 2 microarrays to detail the global programme of gene expression underlying weakly and highly invasive breast cancer cells derived from the human breast cancer cell line MCF7.
2011-12-10 | GSE17889 | GEO
Project description:Promoter methylation is able to induce downregulation of gene expression. 5-Aza-2'-deoxycytidine(Aza), methytransferase inhibitor, induce CpG demethylation. Here, 5-Aza-2'-deoxycytidine(Aza) is treated in a human breast cancer cell, MCF7, for detection of gene expression change.
2011-08-18 | GSE31441 | GEO
Project description:Arsenic is reportedly a biphasic inorganic compound for its toxicity and anticancer effects in humans. Recent studies have shown that certain arsenic compounds including arsenic hexoxide_x000D_ (AS4O6; hereafter, AS6) induce programmed cell death and cell cycle arrest in human cancer cells and murine cancer models. However, the mechanisms by which AS6 suppresses cancer cells are incompletely understood. In this study, we show markedly differential effects of AS6 on cytotoxicity and gene expression in human mammary epithelial normal cells (HUMEC) and Michigan Cancer Foundation 7 (MCF7), a human mammary epithelial cancer cell line. AS6 selectively arrests cell growth and induces cell death in MCF7 cells without affecting the growth of HUMEC in a dose-dependent_x000D_ manner. AS6 alters the transcription of a large number of protein-coding genes in MCF7 cells, but much fewer genes in HUMEC. Importantly, we found that the cell proliferation, cell cycle, and DNA repair pathways are significantly suppressed whereas cellular stress response and apoptotic pathways_x000D_ increase in AS6-treated MCF7 cells. Together, we provide the first evidence of differential effects of AS6 on normal and cancerous breast epithelial cells, suggesting that AS6 at moderate concentrations induces cell cycle arrest and apoptosis through modulating genome-wide gene expression, leading to compromised DNA repair and increased genome instability selectively in human breast cancer cells
2021-02-17 | GSE157574 | GEO
Project description:Human mesenchymal stem cell (MSC)-conditioned medium (CM) was previously reported to affect the biology of tumor cells; however, the precise mechanisms remain unclear. Here, we show that MSCs secreted 40- to 100-nm particles, which have the typical characteristics of exosomes, and these MSC-derived exosomes promoted migration of the breast cancer cell line MCF7. To further investigate the effect of MSC-exosomes on MCF7, we analyzed the gene expression profiles of MCF7 treated with or without MSC-exosomes for 24 h. Investigation of whole genome gene expression level changes in breast cancer cell line MCF7 which were treated with or without mesenchymal stem cell-derived exosomes. This study uses total RNA recovered from two samples. One sample is MCF7 treated with PBS for 24 hours and another one is MCF7 treated with mesenchymal stem cell-derived exosomes for 24hours. The ultimate concentration of mesenchymal stem cell-derived exosomes used in this experiment was 400ng/ul.
2013-05-20 | E-GEOD-46950 | biostudies-arrayexpress
Project description:Identification of TRPS1 interactors in MCF7 breast cancer cell line.
2018-07-17 | PXD010312 | Pride
Project description:Aerobic glycolysis is a hallmark of cancer glucose metabolism. Here we suggest that extracellular vesicles (EVs) originating from cancer cells can modulate glucose metabolism in the recipient cancer cells and induce cell proliferation and aggressive cancer phenotypes. Two breast cancer cell lines with different levels of glycolytic activity, MDA-MB-231 and MCF7, were selected and co-cultured, as the originating and recipient cells. The change in 18F-fluorodeoxyglucose (FDG) uptake of the recipient MCF7 cells was assessed after co-culture with the MDA-MB-231 cells. Proteomics analysis was performed to investigate the changes in the protein expression patterns in the recipient MCF7 cells. FDG uptake by the recipient MCF7 cells was sig-nificantly increased after co-culture with the MDA-MB-231 cells.
2022-02-16 | PXD028806 | Pride