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: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: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: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:We report that EVs originated from cancer cells can modulate glucose metabolism in the recipient cancer cells and induce cell proliferation and aggressive phenotype. Two breast cancer cell lines with different levels of glycolytic activity, MDA-MB-231 of a claudin low-type breast cancer cell and MCF7 of luminal type breast cancer cell, were selected and co-cultured, as the originating and recipient cells using indirect co-culture system such as transwell system or microfluidic system. Proteomic profiling of the co-cultured MCF7 cells revealed proliferation and dedifferentiation of the MCF7 cells following co-culture with the MDA-MB-231 cells. Transcriptomic analysis demonstrated that glycolysis increased in the co-cultured MCF7 cells, and the component analysis of glycolysis-related genes revealed that the second-most component after cytoplasm was extracellular exosomes. In addition, 36 significant KEGG pathways were identified in a total of 856 proteins identified by proteomin analysis of MDA-MB-231-induced EVs. Among these pathways were the main pathways (glycolysis/gluconeogenesis, pyruvate metabolism, and PI3K-Akt signaling pathways) that could explain the metabolic modulation of MCF7 cells. In our work, we indirectly show that it is MDA-MB-231-derived EVs that play an important role in this phenomenon. Our study highlights the potential effects of aggressive cancer cells on other surrounding cancer cells through EVs.
Project description:We cultured human lung and breast cancer cell lines, A549, H23, MDA-MB-231, MCF-7-TNR, and T47D cells. Total RNA was extracted and processed for RNA-SEQ.
