Project description:RNA-sequencing data from MDA-MB231 breast cancer cells, U87MG glioblastoma cells, and mouse breast cancer PDX models treated with antisense oligonucleotides targeting exon 2 of TRA2B. Additionally, RNA-sequencing data from MDA-MB231 breast cancer cells and U87MG glioblastoma cells treated with siRNAs targeting TRA2B. RNA-sequencing data from MDA-MB231 breast cancer cells nad U87MG glioblastoma cells treated with antisense oligonucleotides targeting exon 2 of TRA2B.
Project description:Here, we performed N-glycoproteomics on six triple negative breast cancer cell lines (commercially available cell lines: HCC1187, HCC1937, MDA-MB157, MDA-MB231, MDA-MB436, MDA-MB468) and five normal control cell lines (commercially available MCF10A and 4 non-immortalized human mammary epithelial cells: HMEC_RM10, HMEC_RM1, HMEC_RM2, HMEC_HB5) using hydrazide-based enrichment. Quantitative proteomics and integrative data mining led to the discovery of Plexin B3 (PLXNB3) as a previously undescribed TNBC-enriched cell surface protein.
Project description:RNA-seq data from human MDA-MB231 breast cancer cells expressing control or TRA2B-targeting shRNAs grown for 8 days in 3D culture in matrigel
Project description:Mfng, a modulator of Notch signaling, is highly expressed in human claudin-low breast cancer (CLBC). To determine Mfng’s roles in CLBC pathogenesis,we knocked down Mfng in a CLBC cell line MDA-MB231, and found that Mfng knockdown altered Notch activation, decreased tumor sphere formation in vitro, and reduced tumor growth in xenograft model. To identify the potential downstream targets of Mfng during CLBC tumorigenesis, we compared the gene expression profiles between xenografts tumor derived from of MDA-MB231 cells carrying Mfng shRNA and the control vector. Mfng, a modulator of Notch signaling, is highly expressed in human claudin-low breast cancer (CLBC). To determine Mfng’s roles in CLBC pathogenesis,we knocked down Mfng in a CLBC cell line MDA-MB231, and found that Mfng knockdown caused alteration in Notch activation, associated with decreased tumor sphere formation in vitro, as well as reduced tumor growth in xenograft model. We intend to compare gene expression profiles between xenografts of MDA-MB231 cells carrying Mfng shRNA and the control vector. This project seeks to identify potential downstream targets of Mfng in CLBC.
Project description:We studied the crosstalk between tumor and endothelial cells to explore the role of tumor microenvironment on cancer growth and progression. As part of our investigation, we showed that contact-dependent interaction of endothelial cells with breast tumor cells triggered the differential expression of a large number of genes in endothelium. Endothelial and MDA-MB231 cells were co-cultured together under serum- cytokine-free environment for 5 days followed by sorting endothelial cells and extracting RNA for microarray analysis. All conditions were made in triplicate. Endothelial cells were obtained using the methods described in Seandel M. & Butler J.M., 2008. WCMC-Q Genomics Core
Project description:To determine the absolute copy number of proteins in MDA-MB231 breast cancer cells, we employed IBAQ mediated absolute quantification of proteins based on (Schwanhäusser et al., Nature, 2011), with some modifications. Maqquant calculated iBAQ values were calibrated using spike-in standards, and used to calculate copy numbers for each identified protein within the dataset. Copy numbers for a total of 3,584 proteins were calculated in MDA-MB231 cells.
Project description:We analysed the impact of LARP6 depletion on the proteome of actively growing MDA-MB231 breast cancer cells by SILAC. For this purpose, Light (L) SILAC-labelled MDA-MB231 cells were treated with non-targeting control (NT) or two independent LARP6 siRNA (18i & 97i) for 72 hrs, before lysis in 4% SDS, 100mM Tris/HCl pH 7.5. In parallel, Heavy (H)SILAC labelled non-transfected MDA-MB231 cells were grown and lysed similarly. Each L labeled lysate was then mixed with an equal amount of H labelled lysate. Mixing of samples to the same H standard therefore allowed cross-comparison of different siRNA treatments from separate runs.
Project description:Mfng, a modulator of Notch signaling, is highly expressed in human claudin-low breast cancer (CLBC). To determine Mfng’s roles in CLBC pathogenesis,we knocked down Mfng in a CLBC cell line MDA-MB231, and found that Mfng knockdown altered Notch activation, decreased tumor sphere formation in vitro, and reduced tumor growth in xenograft model. To identify the potential downstream targets of Mfng during CLBC tumorigenesis, we compared the gene expression profiles between xenografts tumor derived from of MDA-MB231 cells carrying Mfng shRNA and the control vector. Mfng, a modulator of Notch signaling, is highly expressed in human claudin-low breast cancer (CLBC). To determine Mfng’s roles in CLBC pathogenesis,we knocked down Mfng in a CLBC cell line MDA-MB231, and found that Mfng knockdown caused alteration in Notch activation, associated with decreased tumor sphere formation in vitro, as well as reduced tumor growth in xenograft model. We intend to compare gene expression profiles between xenografts of MDA-MB231 cells carrying Mfng shRNA and the control vector. This project seeks to identify potential downstream targets of Mfng in CLBC. MDA-MB231 cells were transfected with shRNA against MFNG. Stable cell clones with knockdown of MFNG or corresponding control were selected and injected orthotopically into SCID mice. Total RNA was then extracted from the xenograph tumors for microarray analysis.
