Project description:Transcriptional profiling of the human breast cancer cells and primary breast cancer-associated fibroblasts exposed to compressive stress. Four subtypes of breast cancer cells (BT-474, MCF7, SK-BR-3, MDA-MB-231) and four cases of primary breast cancer-associated fibroblasts (CAF1, CAF2, CAF3, and CAF4) were exposed to a static compressive stress for 24 h.
Project description:Transcriptional profiling of human breast cancer brain metastasis cells (MDA-MB-231Br) comparing control cells with cells with overexpression of LRRC31 gene.
Project description:The cytokine Oncostatin M (OSM) promotes cancer progression by acting as central node for multicellular interactions between cancer cells and surrounding stromal cells. OSM is mainly secreted by myeloid cells and the oncostatin M receptor (OSMR) is expressed by cancer cells and cancer associated fibroblasts (CAFs), among others. To understand the effect of OSM in triple negative breast cancer cells, a small and well-annotated Clariom S gene microarray was performed in OSM-overexpressing (MDA-MB-231-hOSM) and control (MDA-MB-231-hC) MDA-MB-231 cells.
Project description:Description A phase II metabolic enzyme, NAT1 is frequently upregulated in breast cancers. Previous studies have shown that inhibition or depletion of NAT1 in breast cancer cell lines leads to growth retardation both in vitro and in vivo, suggesting that NAT1 contributes to rapid growth of breast cancer cells. This project evaluated the effects of NAT1 knockdown on the proteome of a breast cancer cell line.hese groups include a parental MDA-MB-231 breast cancer cells and two separate NAT1 knockout (KO) cell lines differing by proliferation rates.
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:Background Breast cancer is the leading cause of cancer related deaths in women. Triple negative breast cancers are highly aggressive, have an overall poor prognosis and has limited therapeutic options. Previously, we have identified an environmental induced gene mdig that predicted the overall survival in breast cancer patients and regulated breast cancer cell growth, motility and invasion partially through DNA and histone methylation. Mdig’s role in breast cancer growth and motility has been revealed however a comprehensive analysis of the proteomic profile of mdig affected cells in triple negative breast cancer has not been attempted yet. Methods We applied mass spectrometry technology featuring global proteomics and post translational modifications in triple negative breast cancer cells MDA-MB-231 that were deleted for mdig via CRISPR Cas 9 gene editing. Using label-free bottom up quantitative proteomics, we compared the proteomes of wildtype control (WT) and mdig knockout (KO) MDA-MB-231 cells and identified the proteins and pathways that are significantly altered with mdig deletion. Ingenuity Pathway Analysis (IPA) platform was further used to explore the signaling pathway networks with differentially expressed proteins and identified top canonical pathways, upstream regulators, and causal disease networks. Results 904 differentially expressed (p < 0.005) proteins were identified in MDA-MB-231 cells knocked out for mdig. Post-translational modification (PTM) analysis indicated that mdig loss reduced the abundance of oxidized histidine 39 of 60S ribosomal protein L27a (q = 0.00030) whereas global abundance of di-methylated lysine containing peptides was increased (p = 0.02). Relevance Our data provides the first insight towards the protein expression pattern in breast cancer associated with a complete disruption of the mdig gene. Differentially expressed proteins between WT and KO MDA-MB-231 triple negative breast cancer cells provided substantial information regarding the key proteins, biological process and pathways that are specifically upregulated in breast cancer tumorigenicity and invasiveness. Mdig affected signaling pathways and hub molecules will benefit for the development of novel treatment strategies for the development of breast cancer therapies.
Project description:We performed gene expression profiling on the MDA-MB-231 and MDA-MB-436 human breast cancer cell lines following siRNA-mediated inhibition of Fn14 expression as an approach to identify the mechanistic basis for Fn14 regulation of invasive capacity. Keywords: siRNA-mediated inhibition
Project description:We analyzed the miRNA expression in 6 breast cancer cell lines from young (HCC1500, HCC1937) and old (MCF-7, MDA-MB-231, HCC1806 and MDA-MB-468) patients with breast cancer using the GeneChip® miRNA 2.0 Array (Affymetrix, Santa Clara, CA, USA).