Project description:Aurora Kinase B and ZAK interaction model
Equivalent of the stochastic model used in "Network pharmacology model predicts combined Aurora B and ZAK inhibition in MDA-MB-231 breast cancer cells" by Tang et. al. 2018.
The only difference is cell division and partitioning of the components, which are available in the original model for SGNS2.
Project description:Mesenchymal stromal cells were cultured in 3D PEG hydrogels for 7 days in the presence of serum-free media or conditioned media from a panel of breast cancer cells (MCF-7, MDA-MB-231, MDA-MB-231 lung-tropic, MDA-MB-231 brain-tropic, MDA-MB-231 bone-tropic). In all cases, the secretomes were collected after cancer cells were in serum-free media for 24h.
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).
Project description:Aerobic glycolysis is a hallmark of cancer glucose metabolism. Here we suggest that extracellular vesicles (EVs) originating from cancer cells can modulate glucose metabolism in the recipient cancer cells and induce cell proliferation and aggressive cancer phenotypes. Two breast cancer cell lines with different levels of glycolytic activity, MDA-MB-231 and MCF7, were selected and co-cultured, as the originating and recipient cells. The change in 18F-fluorodeoxyglucose (FDG) uptake of the recipient MCF7 cells was assessed after co-culture with the MDA-MB-231 cells. Proteomics analysis was performed to investigate the changes in the protein expression patterns in the recipient MCF7 cells. FDG uptake by the recipient MCF7 cells was sig-nificantly increased after co-culture with the MDA-MB-231 cells.
Project description:Nuclear LASP-1 has a direct correlation with the overall survival of breast cancer patients. Gene expression analysis of MDA-MB-231S (sorted for high surface expression of CXCR4) and MDA-Bone-Un (Mouse bone metastasized MDA-MB-231 cells) human basal-like breast cancer cells cultured in 3D-Matrigel was performed. Changes in transcript levels of key microRNAs 29B1 and 29B2, miRLet7F1, miR519A1, MMP9, MMP1, FAM75D4, Interferons a7 and a17, Glycine receptor a3, CADM2 and claudin12 Non-silencing (control) and LASP-1 knock down MDA-MB-231-S and MDA-Bone-Un cells were cultured on 3D-Matrigel, total RNA was extracted and analyzed - 1 biological replicate each
Project description:To investigate the function of Neuropilin-1 (NRP-1) in breast cancer MDA-MB-231 cells. CRISPR-Cas9 gene editing was used to knockout (KO) the NRP-1 gene in MDA-MB-231 human triple-negative breast cancer cells. Differentially expressed genes (DEGs) were determined in NRP-1 KO and parental MDA-MB-231 cells using whole transcriptome next-generation sequencing.
Project description:We cultured the ER negative breast cancer cell line MDA-MB-231 and the ER positive breast cancer cell line MCF7 in serine-free media for 24h. RNA was extracted from the cells and submitted for RNA sequencing.
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:PAD4 is overexpressed in many cancer cells. We developed PAD inhibitors that efficiently inhibit the cancer cell growth. One inhibitor YW3-56 could efficiently induce cell death of triple negative breast cancer MDA-MB-231 cells. We used microarray to detail the global gene expression of MDA-MB-231 before and after YW3-56 treatment and identify significant up-regulated or down-regulated genes by YW3-56 MDA-MB-231 cells were cultured and treated with vehicle (DMSO) or YW3-56. Cells were washed with PBS and harvested for RNA extraction and hybridization on Affymetrix microarray.
