Project description:Breast cancer invasive growth, metastasis and therapeutic resistance affects the clinical ourcome. We explored the epigenetic mechanisms that control these process in breast cancer cell line, MDA-MB-231 by knocking down a lysine specific demethylase KDM3A We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process. Human breast cancer cell line MDA-MB-231 was infected with scramble or KDM3A shRNA. After selection, the cells were used for microarray analysis.
Project description:Copy number gain/amplification of SETDB1 has been found in several human cancers, but the detailed oncogenic mechanism(s) of SETDB1 contributing to breast cancer remains largely unexplored. In this project, we analyzed the transcriptome of human breast cancer cell lines (MDA-MB-231 and MDA-MB-453) upon silencing of SETDB1 to explore the potential mechanism(s) underlying SETDB1 promoted breast cancer. In MDA-MB-231 cells, SETDB1 was silenced by shRNA-1. In MDA-MB-453 cells, SETDB1 was reduced by shRNA-3.
Project description:This study compares a cell line (MDA-MB-468GFP-LN) that aggressively metastasizes to lymph nodes to its parental line MDA-MB-468GFP. Derivation of the lines is described in Vantyghem et al, Clinical & Experimental Metastasis (2005) 22: 351–361. The goal here was to compare the gene expression profile of MDA-MB-468GFP-LN to MDA-MB-468GFP, Compare differential expression to databases of genes known to be involved in either cancer stem cell identification or lymph node specific metastasis in large scale clinical studies, and to confirm genes by RT-PCR
Project description:The recent success of monoclonal antibody checkpoint inhibitor therapies that enhance the ability of CD8+ T cells to detect cancer-related antigenic peptides has refocused the need to fully understand the repertoire of peptides being presented to the immune system. Whilst the peptide ligandome presented by cell surface HLA class I molecules on cancer cells has been studied extensively, the ligandome of extracellular vesicles remains poorly defined. Here we report the HLA class I ligandome of both cell surface and extracellular vesicles from eight breast cancer cell lines (MCF7, MDA-MB-231, MDA-MB-361, MDA-MB-415, MDA-MB-453, HCC 1806, HCC 1395, and HCC 1954), and additionally the melanoma cell line ESTDAB-056 and the multiple myeloma line RPMI 8226. Utilising HLA class I immunoisolation and mass spectrometry we detected a total of 6574 peptides from the cell surface and 2461 peptides from the extracellular vesicles of the cell lines studied. Within the extracellular vesicle HLA class I ligandome we identified 150 peptides derived from tumour associated antigenic proteins, of which 19 peptides have been shown to elicit T cell responses in previous studies. Our data thus confirms for the first time the presence of clinically relevant tumour-associated antigenic peptides in the HLA class I ligandome present on EV.
Project description:To identify the downstream target genes of PUS1 on breast cancer cells, we established MDA-MB-231 cell lines in which PUS1 has been knocked down by shRNA. We then performed gene expression profiling analysis using data obtained from RNA-seq of PUS1 knockdownMDA-MB-231 cells as well as negative control shRNA group
Project description:To investigate the cooperative function HJURP/YAP1/NDRG1 in the regulation of progression in triple negative breast cancer, we established MDA-MB-231 cell lines in which each target gene has been knocked down by shRNA. We then performed gene expression profiling analysis using data obtained from RNA-seq of 2 different cells.
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: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.
