Project description:Deleted in breast cancer (DBC1; also known as CCAR2) is a coactivator for nuclear receptors (NRs) as well as a negative regulator of epigenetic modifiers such as deacetylases SIRT1 and HDAC3. We performed genome-wide gene expression analysis in control (shNS) and DBC1-depleted (shDBC1) MDA-MD-231 cells to investigate global gene expression changes induced by depletion of DBC1 Total RNAs were isolated from MDA-MB-231 cells expressing shNS or shDBC1 using the RNeasy mini kit (Qiagen). The integrity of RNA was analyzed using an Agilent 2100 Bioanalyzer. Two independent biological replicates were assayed for each sample. The microarrays were performed following the Affymetrix standard protocol.
Project description:Deleted in breast cancer (DBC1; also known as CCAR2) is a coactivator for nuclear receptors (NRs) as well as a negative regulator of epigenetic modifiers such as deacetylases SIRT1 and HDAC3. We performed genome-wide gene expression analysis in control (shNS) and DBC1-depleted (shDBC1) MDA-MD-231 cells to investigate global gene expression changes induced by depletion of DBC1
Project description:CCAR2 has been characterized as a key regulator of physiological and pathophysiological activities, such as DNA damage, senescence and tumorigenesis. However, the mechanism by which the functional stability of CCAR2 is regulated has yet to be elucidated. We performed Next Generation Sequencing analysis in wild-type and CCAR2 knockout MDA-MB-231 cells to investigate global gene expression changes under normal or hypoxic condition.
Project description:Analysis of the effect of shRNA-mediated knockdown of SOX4 on global gene expression levels in MDA-MB-231 human breast cancer cells. Results were used for the identification of overlapping up- and downregulated genes in TRPM7 + SOX4 shRNA MDA-MB-231 cells
Project description:To determine the effect ALDH1A3 expression on global gene expression in MDA-MB-231 cells and MDA-MB-468 cells In MDA-MB-231 cells, ALDH1A3 was overexperssed (have low endogenous levels of ALDH1A3) and compared to MSCV empty vector control. In MDA-MB-468 cells that have high endogenous levels of ALDH1A3, ALDH1A3 expresion was reduced with ALDH1A3 shRNA1 and compared to scramble shRNA control.
Project description:Deleted in breast cancer (DBC1; also known as CCAR2) is a coactivator for nuclear receptors (NRs) and other transcription factors as well as a negative regulator of epigenetic modifiers such as deacetylases SIRT1 and HDAC3. We performed genome-wide gene expression analysis in wild-type and DBC1 knockout SW480 cells to investigate global gene expression changes induced by DBC1 knockout.
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.
