Project description:Sepantronium bromide (YM-155) is believed to trigger apoptosis in tumor cells by inducing a major reduction in baculoviral inhibitor of apoptosis repeat-containing 5 (BIRC 5) also known as survivin. In MDA-MB-231 cells, the toxic effects of YM-155 were equi potent to standard chemotherapy drugs , having an LC50 < 50ng/ml. In this study we investigate whole transcriptome changes occurring at 8 hours of incubation with YM-155, preceding apoptosis as well as at a 20 hour time point. Microarrays were acquired for mRNAs and long intergenic non-coding RNA transcripts using the GeneChip™ Human Gene 2.1 ST Arrays by Affymetrix Inc.
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 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.
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: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:To further development of our gene expression approach, we have employed whole genome microarray expression profiling to identify genes related to VEGF in MDA-MB-231 breast cancer cell line.
Project description:To investigate the function ARL11 in the regulation of PARPi resistance, we established MDA-MB-231 cells overexpressing ARL11. We then performed gene expression profiling analysis using data obtained from RNA-seq of ARL11 overexpression or vector control MDA-MB-231 cells treated with or without Olaparib.
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: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:We examined gene expression change under amino acid restriction in JPH203 treated MDA-MB-231 and T-47D cells. JPH203 treatment induced endoplasmic reticulum stress response via amino acid starvation stress pathway in both MDA-MB-231 and T-47D cells. Moreover, MDA-MB-231 was upregulated anti-oxidants related genes.
