Project description:We grew MDA-MB231 cells in a media that had been reconstituted with water that was treated by the Bio-Electric Field Enhancement device generated direct current dielectrophoretic electromagnetic field (Treated group) and cells that were grown in media that was reconstituted with water that was not treated by the BEFE device dc DEP EMF. They were grown for 3 days in each of these media and then analyzed with Affymetrix 2.0 Microarrary Analyses. It was an experimental controlled design.
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: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: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.
Project description:RNA-Seq profiling of triple-negative MDA-MB-231 cell line with know-down of non-canonical WNT signaling receptor Ror1. The MDA-MB231 cells were either transfected with a non-sense control shRNA (shCTL) or with a ROR1 shRNA (shROR1) construct. The objective was to find expression-responsive targets of these perturbations as potential drivers of MDA-MB231 cell invasiveness.
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:Experiments to test the effect of CtBP2 inhibition on metabolism of breast cell lines. In particular, experiment 1 involves comparison between a normal breast cell line (MCF102A) and a triple-negative breast cancer cell line (MDA-MB231). Experiment 2 is a study between MDA-MB231 silenced for CtBP2 by stable RNA interference (shCtBP2 cells) compared to scramble (shCTRL cells). Experiment 3 is a comparison between a normal breast cell line (MCF102A) and a triple-negative breast cancer cell line (MDA-MB231)in the presence of the absence of small-molecule CtBP inhibitors: HIPP (400 μM) or P4 (300 μM)for 48 hours.