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:Knock-down of LSD1 using siRNA approach induced regulation of several proliferation-associated genes in ER-negative breast cancer cells MDA-MB-231.
Project description:Identification of open chromatin regions in wildtpye, control knock-down (shCtrl) and ZEB1 knock-down (shZEB1) human breast cancer MDA-MB-231 cells by ATAC(Assay for transposable-accessible chromatin)-seq.
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:We describe here the proteome of the human breast cancer cell line MDA-MB-231 expressing normal levels of the lncRNA NORAD, or after knock-down NORAD with siRNA and LNA gapmers.
Project description:RhoGDIbeta (ARHGDIB) is often expressed in tumor cells. It negatively regulates Rho-GTPases, but may have other functions as well. To analyze its effect on gene expression, RhoGDIbeta was suppressed by RNA interference in MDA-MB-231 breast cancer cells and changes in gene expression monitored by cDNA microarrays. Keywords: siRNA knock-down analysis
Project description:Epithelial-to-mesenchymal transition (EMT) is a fundamental process in development and disease. If aberrantly activated it is a trigger for tumour progression and metastasis (Thiery et al 2009 Cell). It is now known that EMT activation is also associated with the maintenance of stem-cell properties (Mani et al. 2008 Cell). Since Zinc-finger enhancer binding transcription factor 1 (ZEB1) is a crucial EMT activator, we analyzed the changes in the gene expression profile that accompany shRNA mediated loss of ZEB1 in MDA MB 231 basal type breast cancer cells. MDA MB 231 is a cell line that exhibits mesenchymal characteristics, but reverts to an epithelial phenotype upon ZEB1 knock down (Spaderna et al. 2008 Cancer Research). MDA MB 231 cells were stably transfected with control (GFP) or ZEB1 shRNA. Upon puromycin selection, single cell clones were picked and characterized. Cells from two control versus two ZEB1 knockdown clones were harvested, total RNA was isolated and processed to hybridization.
Project description:RNA-Sequencing of basal subtype triple negative breast cancer cells, MDA-MB-231. MDA-MB-231 cells were lentivirally transduced with pLKO short-hairpin (sh) luciferase control or shZnf148 in triplicates. Differentially expressed genes by the shRNA compared to the control were determined.
Project description:Knock-down of LSD1 using siRNA approach induced regulation of several proliferation-associated genes in ER-negative breast cancer cells MDA-MB-231. To identify changes on gene expression caused by treatment with siRNA directed against LSD1 (si) or control siRNA (control) in MDA-MB-231 cells, total RNA was purified from the cells after treatment for 6 days (2 rounds of transfection). Three biological replicates were used.
Project description:p63 ChIP-SEQ in a p63 expressing basal-subtype breast cancer cell line, MCFDCIS and in a p63 deficient claudin-low subtype breast cancer cell line, MDA-MB-231 p63 ChIP-SEQ on MCFDCIS and MDA-MB-231 cell lines
