Project description:To identify gene expression changes associated with treatment of EVs from MDA-MB-231 [231] and MCF10A [10A] cells) in NIH3T3 cells, we analyzed RNA isolated from PBS- or EV-treated NIH3T3 cells. Gene expression in NIH3T3 cells treated with EV from MDA-MB-231 cells was compared to cells treated with PBS or EV from MCF10A cells, both of which served as controls in this experiment.
Project description:1. Quantitative Proteomics: MDA-MB-231, MDA-MB-468, and MCF12A cells were treated with DMSO (vehicle control) or SU056 (novel small molecule drug candidate). Quantitative proteomics analysis was performed on cell lysates. 2. Cellular Thermal Shift Assay (CETSA): MDA-MB-231 cells were treated with DMSO or SU056 and incubated at different temperatures and protein differences in the resulting soluble and insoluble fractions were determined.3. Cellular Thermal Shift Assay (CETSA): MDA-MB-231 YBOX1 KD cells were treated with DMSO or SU056 and incubated at different temperatures and protein differences in the soluble fractions were determined.
Project description:To investigate mechanism of inosine promotes the survival and metabolism of MDA-MB-231 cells under starvation conditions, MDA-MB-231 cells were treated with inosine and glucose for 12h under starvation conditions. We then performed gene expression profiling analysis using data obtained from RNA-seq of MDA-MB-231 cells under three different treatments(-G-Q,Inosine,Glucose).
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.
Project description:To examine the role of NONO in estrogen-independent breast cancer, MDA-MB-231 cells were treated with siRNA targeting NONO or control siRNA (siControl). Microarray analysis revealed NONO-regulated genes in MDA-MB-231 cells.