Homo sapiens
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-33827
PROVIDER: PRJNA148199 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Small-molecule Smac mimetics target inhibitor of apoptosis (IAP) proteins to induce TNFα-dependent apoptosis in cancer cells and several Smac mimetics have been advanced into clinical development as a new class of anticancer drugs. However, preclinical studies have shown that only a small subset of cancer cell lines are sensitive to Smac mimetics used as single agents and these cell lines are at risk of developing drug resistance to Smac mimetics. Thus, it is important to understand the molecular mechanisms underlying intrinsic and acquired resistance of cancer cells to Smac mimetics in order to develop effective therapeutic strategies to overcome or prevent Smac mimetic resistance. We established Smac mimetic resistant sublines derived from MDA-MB-231 breast cancer cells, which exhibit exquisite sensitivity to the Smac mimetic SM-164, and used microarrays to detail the global programme of gene expression underlying SM-164 resistance in MDA-MB-231 cells and identified differentially expressed genes in SM-164-resistant and -sensitive MDA-MB-231 cells. SCID mice with MDA-MB-231 xenograft tumors were treated with 5 mg/kg of SM-164 intravenously for 5 days/week for 2 weeks. SM-164-regressed MDA-MB-231 tumors regrew after treatment ended. Tumor cells from these regrown MDA-MB-231 tumors were isolated and total RNAs were prepared for microarray analysis.
2012-03-01 | E-GEOD-33827 | biostudies-arrayexpress
Project description:Small-molecule Smac mimetics target inhibitor of apoptosis (IAP) proteins to induce TNFα-dependent apoptosis in cancer cells and several Smac mimetics have been advanced into clinical development as a new class of anticancer drugs. However, preclinical studies have shown that only a small subset of cancer cell lines are sensitive to Smac mimetics used as single agents and these cell lines are at risk of developing drug resistance to Smac mimetics. Thus, it is important to understand the molecular mechanisms underlying intrinsic and acquired resistance of cancer cells to Smac mimetics in order to develop effective therapeutic strategies to overcome or prevent Smac mimetic resistance. We established Smac mimetic resistant sublines derived from MDA-MB-231 breast cancer cells, which exhibit exquisite sensitivity to the Smac mimetic SM-164, and used microarrays to detail the global programme of gene expression underlying SM-164 resistance in MDA-MB-231 cells and identified differentially expressed genes in SM-164-resistant and -sensitive MDA-MB-231 cells.
2012-03-01 | GSE33827 | GEO
Project description:Expression data from MDA-MB-231 parental and xenograft tumor cells treated with Smac mimetic SM-164.
2015-08-18 | E-GEOD-33827 | ExpressionAtlas
Project description:RNA was isolated from ectopically sFRP1-expressing MDA-MB-231 cells and control MDA-MB-231 cells and as well from tumor lysates arising from these cells as nude mouse xenograft. Gene expression profiles for these samples were investigated using Affymetrix arrays. Experiment Overall Design: MDA-MB-231 human breast cancer cells were stably transfected with human sFRP1 encoding vector or empty vector as control. After the selection with antibiotics, three clones of MDA-MB-231/sFRP1 and three clones of MDA-MB-231/control were selected. These six clones were cultured individually in DMEM 10% FCS with 1mg/ml G-418. When cells reached 70-80% confluence, RNA was isolated from the cells. In parallel, the three clones of MDA-MB-231/sFRP1 and the three clones of MDA-MB-231/control were pooled respectively. One million of cells from each pool were suspended in 100ul PBS and injected to fat pads of female balb/c nude mice (6 mice were injected with MDA-MB-231/sFRP1 and 5 mice were injected with MDA-MB-231/control) to do a xenograft experiment. A few - several weeks after, mice were sacrificed when tumor reached a certain size, tumors were taken and RNA was isolated using trizol reagent.
2009-05-11 | E-GEOD-13806 | biostudies-arrayexpress
Project description:Identifying the gene expression alterations that occur in both the tumor and stroma is essential to understanding tumor biology. We have developed a dual-species microarray analysis method that allows the dissection of both tumor and stromal gene expression profiles from xenograft models, based on limited interspecies cross-hybridization on Illumina gene expression beadchips. This methodology allows for simultaneous genome-wide analysis of gene expression profiles of both tumor cells and the associated stromal tissue. Data is provided regarding the crosshybridization of mouse liver RNA on human microarray, and MDA-MB-231 breast cancer cell line RNA on mouse microarray. Data is also provided for comparisons of MDA-MB-231 gene expression in vitro vs. in vivo, and mouse liver gene expression in control mice vs. stroma from MDA-MB-231 xenograft liver metastasis in tumor bearing mice A total of 18 samples were analyzed. Samples consist of 6 different types with each type in triplicate. Types are (1) MDA-MB-231 cell line grown in vitro and arrayed on mouse chips, (2) mouse liver from NOD/SCID mice arrayed on human chips, (3) MDA-MB-231 cell line grown in vitro arrayed on human chips, (4) MDA-MB-231 xenograft liver metastasis arrayed on human chips, (5) mouse liver from NOD/SCID mice arrayed on mouse chips, and (6) MDA-MB-231 xenograft liver metastasis arrayed on mouse chips. The overall design had three objectives: (1) to determine crosshybridizing probes based on sample types 1, 2, 3, and 5, (2) detect stromal and tumor expression using sample types 4 and 6, and (3) determine genes differentially expressed in tumor or metastasis compared to normal by comparing sample types 3 and 4 and comparing sample types 1 and 5.
2011-11-22 | E-GEOD-30993 | biostudies-arrayexpress
Project description:RNA was isolated from ectopically sFRP1-expressing MDA-MB-231 cells and control MDA-MB-231 cells and as well from tumor lysates arising from these cells as nude mouse xenograft. Gene expression profiles for these samples were investigated using Affymetrix arrays.
2009-05-01 | GSE13806 | GEO
Project description:Identification of genes that are involved in self-seeding by comparing gene expression profiles between parental MDA-MB-231 cells and seeder cells (MDA-231-S1a and S1b) 2 replicates from each sample (parental MDA-MB-231, MDA-MB-231 S1a and MDA-MB-231 S1b) were analyzed
2010-04-07 | E-GEOD-18833 | biostudies-arrayexpress
Project description:The project profiled the expression patterns in hypoxia induced secretomes between MDA-MB-231 parental and MDA-MB-231 Bone Tropic (BT) breast cancer cell lines which have been previously generated by Massague and colleagues (Kang et al. Cancer Cell 2003).
2017-03-29 | MSV000080797 | MassIVE
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.
2021-09-22 | ST001920 | MetabolomicsWorkbench
Project description:The project profiled the expression patterns in hypoxia induced secretomes between MDA-MB-231 parental and MDA-MB-231 Bone Tropic (BT) breast cancer cell lines which have been previously generated by Massague and colleagues (Kang et al. Cancer Cell 2003).
2015-05-28 | PXD000397 | Pride