Project description:To examine the role of NONO in estrogen-independent breast cancer, MDA-MB-231 cells were treated with siRNA targeting NONO or control siRNA (siControl). Microarray analysis revealed NONO-regulated genes in MDA-MB-231 cells.
Project description:We explore the NF-κB responsive transcription that was regulated by Uc003xsl.1/NKRF complex. The chromatin immunoprecipitation coupled with high-throughput sequencing (ChIP-seq) was performed for NKRF in MDA-MB-231-P3 cells treated with si-Uc003xsl.1 or control siRNA. The ChIP-seq data displayed 3604 peak calls in MDA-MB-231-P3 cells against control siRNA and were primarily identified as NF-κB targeting genes.
Project description:Quantification of lipid species from cultured human MDA-MB-231 and BT549 cells with or without siRNA knockdown of ACSL1 and treated or not with eleostearic acid
Project description:MDA-MB-231 are a metastatic triple-negative breast cancer cell line that bears a missense p53 mutation (R280K). We depleted endogenous mutp53 in MDA-MB-231 cells by siRNA transfection, and treated the cells with Tumor Necrosis Factor (TNF)-alpha. Microarray analysis was performed to evaluate the impact of mutant p53 on the transcriptional response triggered by TNFα in these cells. MDA-MB-231 cells transfected with control or p53 siRNA were treated with TNFα for 20 hrs or left untreated. The study comprises four experimental points, each in triplicate.
Project description:Alternative splicing—the production of multiple mRNA isoforms from a single gene—is regulated in part by RNA-binding proteins (RBPs). While the RBPs Tra2? and Tra2? have both been implicated in the regulation of alternative splicing, their relative contribution to this process are not well understood. Here we use iCLIP to identify Tra2? target exons in MDA-MB-231 cells. We find that simultaneous—but not individual—depletion of Tra2? and Tra2? induces substantial shifts in the splicing pattern of endogenous Tra2? target exons identified by iCLIP. We next use RNA-seq following joint Tra2 protein depletion to comprehensively identify Tra2 protein-dependent exons in MDA-MB-231 cells. Endogenous Tra2? binding sites were mapped across the MDA-MB-231 cell transcriptome in biological triplicate iCLIP experiments. RNA-seq was performed using three biological replicates of negative control siRNA treated MDA-MB-231 cells and three biological replicates of TRA2A and TRA2B siRNA treated MDA-MB-231 cells.
Project description:1. Quantitative Proteomics: MDA-MB-231, MDA-MB-468, and MCF12A cells were treated with DMSO (vehicle control) or SU056 (novel small molecule drug candidate). Quantitative proteomics analysis was performed on cell lysates. 2. Cellular Thermal Shift Assay (CETSA): MDA-MB-231 cells were treated with DMSO or SU056 and incubated at different temperatures and protein differences in the resulting soluble and insoluble fractions were determined.3. Cellular Thermal Shift Assay (CETSA): MDA-MB-231 YBOX1 KD cells were treated with DMSO or SU056 and incubated at different temperatures and protein differences in the soluble fractions were determined.
Project description:To examine the role of long non-coding RNA TMPO-AS1 in breast cancer, MDA-MB-231 cells were treated with siRNAs targeting TMPO-AS1 (siTMPO-AS1) or control siRNA (siControl). 3 samples
Project description:MDA-MB-231 cell line with relatively high DOT1L levels was treated with two potent, selective inhibitors of the DOT1L histone methyl transferase. These compounds can inhibit cells migration and invasion and induce differentiation. Here we provide expression profiling data of cells treated with two DOT1L inhibitors [1] [2], DOT1L siRNA (siDOT1L) or control.
Project description:To investigate the function ARL11 in the regulation of PARPi resistance, we established MDA-MB-231 cells overexpressing ARL11. We then performed gene expression profiling analysis using data obtained from RNA-seq of ARL11 overexpression or vector control MDA-MB-231 cells treated with or without Olaparib.
Project description:In the article "Fra-1 regulates its target genes via binding to remote enhancers without exerting major control on chromatin architecture in triple negative breast cancers" by Bejjani et al., we mapped p300/CBP binding sites in MDA-MB-231 cells transfected with a control siRNA or a siRNA directed against Fra-1(FOSL1) to study whether Fra-1 can modulate p300/CBP recruitment on MDA-MB-231 genome
