Project description:Dicer, RNase III endonuclease, is an essential enzyme in miRNA biogenesis that regulates target gene expression, and it has been reported that aberrant expressions of Dicer associate with the clinical outcomes of patients in various cancers. To explore the miRNA differencial expression regulated by Dicer in MDA-MB-231/E1A cells, the microarray profiling analysis was employed to conduct differentially expressed miRNAs in stable MDA-MB-231/vector, MDA-MB-231/E1A, and MDA-MB-231/E1A/shDicer cells. The four groups including vector control, E1A-expressing and Dicer knockdown in E1A-expressing MDA-MB-231 cells were harvested and RNA were isolated. Two independent experiments were performed for each group.
Project description:Dicer, RNase III endonuclease, is an essential enzyme in miRNA biogenesis that regulates target gene expression, and it has been reported that aberrant expressions of Dicer associate with the clinical outcomes of patients in various cancers. To explore the miRNA differencial expression regulated by Dicer in MDA-MB-231/E1A cells, the microarray profiling analysis was employed to conduct differentially expressed miRNAs in stable MDA-MB-231/vector, MDA-MB-231/E1A, and MDA-MB-231/E1A/shDicer cells.
Project description:We report the high-throughput profiling of histone modifications( H3K4me3 and H3K27ac) inTRIM11 knockdown and KDM5C knockdown MDA-MB-231 cells. we generated genome-wide chromatin-state maps of MDA-MB-231 cells.This study provides the localization of H3K4me3 and H3K27ac on chromatin in TRIM11 knockdown and KDM5C knockdown MDA-MB-231 cells.
Project description:This Series reports results of miRNA profiling of estrogen-receptor-positive (MCF7) and estrogen-receptor-negative (MDA-MB-231) cells. Retinoic Acid (RA) induces mir-21 in MCF-7 but not in MDA-MB-231 cells. MCF-7 and MDA-MB-231 cells were treated (or not) with retinoic acid (RA) and grown for either 6 hours or 48 hours.
Project description:This Series reports results of miRNA profiling of estrogen-receptor-positive (MCF7) and estrogen-receptor-negative (MDA-MB-231) cells. Retinoic Acid (RA) induces mir-21 in MCF-7 but not in MDA-MB-231 cells. MCF-7 and MDA-MB-231 cells were treated (or not) with retinoic acid (RA) and grown for either 6 hours or 48 hours. miRNA profiling: Factorial design 2x2x2 'cube'; main factors: RA, cells, time; interactions: RA.cells, RA.time, cells.time, RA.cells.time.
Project description:Identification of changes in protein expression by label-free shotgun proteomics in breast cancer MDA-MB-231 cells with knockdown of ELOVL5 and IGFBP6 genes in comparison with control MDA-MB-231 cells.
Project description:We report the gene expression patterns in MDA-MB-231 (a line selected for low metastatic ability), MDA-MB-231-1833 (its bone-tropic metastatic derivative line), MDA-MB-231p27CK-DD (a phosphomimetic cell line), MDA-MB-231-1833shp27 (p27 knockdown cell line), MDA-MB-231-1833PF1502 (PI3K inhibitor treatment). It shows that the gene expression pattern are regulated in a p27 phosphorylation-dependent manner.
Project description:To determine the differentially expressed miRNAs in MDA-MB-231-GATA3 cells vs. MDA-MB-231-Control cells Pooled polyclonal cells from MDA-MB-231 breast cancer cells +/- GATA3 over-expression were analyzed for miRNA expression
Project description:To provide preliminary insights into metabolic and lipidomic characteristics in radioresistant triple-negative breast cancer (TNBC) cells and suggest potential therapeutic targets, we performed a comprehensive metabolic and lipidomic profiling of radioresistant MDA-MB-231 (MDA-MB-231/RR) TNBC cells and their parental cells using gas chromatography-mass spectrometry and nano electrospray ionization-mass spectrometry, followed by multivariate statistical analysis. Buthionine sulfoximine (BSO) and radiation were co-treated to radioresistant TNBC cells. The level of glutathione (GSH) was significantly increased, and the levels of GSH synthesis-related metabolites, such as cysteine, glycine, and glutamine were also increased in MDA-MB-231/RR cells. In contrast, the level of lactic acid was significantly reduced. In addition, reactive oxygen species (ROS) level was decreased in MDA-MB-231/RR cells. In the lipidomic profiles of MDA-MB-231/RR cells, the levels of phosphatidylcholine (PC) and phosphatidylethanolamine (PE) were significantly increased, whereas those of most of the phosphatidylinositol species were significantly decreased. BSO sensitized MDA-MB-231/RR cells to radiotherapy, which resulted in decreased GSH level and increased ROS level and apoptosis. Radioresistant TNBC cells showed distinct metabolic and lipidomic characteristics compared to their parental cells. We suggested activated GSH, PC, and PE biosynthesis pathways as potential targets for treating radioresistant TNBC cells. Particularly, enhanced radiosensitivity was achieved by inhibition of GSH biosynthesis in MDA-MB-231/RR cells.
