Project description:To obtain an overview of the cellular functions regulated by ZNF217 signaling in breast-cancer cell lines, we performed global gene-expression profiling on MDA-MB-231-pcDNA6 and MDA-MB-231-ZNF217 cells
Project description:To obtain an overview of the cellular functions regulated by ZNF217 signaling in breast-cancer cell lines, we performed global gene-expression profiling on MDA-MB-231-pcDNA6 and MDA-MB-231-ZNF217 cells Two independent cell-culture replicates from the total population of MDA-MB-231-pcDNA6 and MDA-MB-231-ZNF217 stable transfectants were used to generate total RNA. Total RNA was extracted from cell culture using a Qiagen RNA extraction kit and RNA quality was assessed using the BioAnalyzer 2100™ (Agilent Technologies). Complex probes were produced from these RNA, then hybridized to Human genome U133 Plus 2.0 array according to the manufacturer’s recommendations (Affymetrix).
Project description:The cytokine Oncostatin M (OSM) promotes cancer progression by acting as central node for multicellular interactions between cancer cells and surrounding stromal cells. OSM is mainly secreted by myeloid cells and the oncostatin M receptor (OSMR) is expressed by cancer cells and cancer associated fibroblasts (CAFs), among others. To understand the effect of OSM in triple negative breast cancer cells, a small and well-annotated Clariom S gene microarray was performed in OSM-overexpressing (MDA-MB-231-hOSM) and control (MDA-MB-231-hC) MDA-MB-231 cells.
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.