ABSTRACT: The whole transcriptome expression profiling comparison between the CtBP1 knockdown, CtBP2 knockdown and scramble control in ovarian cancer SKOV3 cells
Project description:To discover the core gene expression features of CtBP1, CtBP2 differently regulated in ovarian cancer SKOV3 cells. The compared the whole transcript expression profiling between CtBP1 knockdown, CtBP2 knockdown and scramble control in ovarian cancer skov3 cells.
Project description:To discover the regulatory role of CTBP1/2 in high grade serous ovarian cancer, The full cDNA was extracted from SKOV3 shRNA control and CtBP1/2 knockdown and then compared the expression profiles of them to discovery the key functions and pathways regulated by CtBP1/2..
Project description:To identify oligomerization dependent interactors of C-terminal binding protein 2 (CTBP2), we stably expressed CTBP2 wild type or a monomeric mutant (CTBP2 mono: CTBP2 C140Y, N144R, R147E, L156W) in Ctbp1-/-, Ctbp2-/- J774.1 cells and profiled their genome-wide interactome in LPS conditions after 3 h of stimulation. Differential profiling of CTBP2’s wild type and monomeric interactome shows oligomer-specific interactions with multiple repressors including KDM1A and the NuRD complex. Conversely, monomers retain the ability to interact with AP-1 and RNA polymerase II.
Project description:Regulation of gene expression by the CtBP family of NADH-sensitive transcriptional regulators, in MCF7 cells under normoxia and hypoxia. To determine the effect of CtBP knockdown on gene expression in MCF7 we transfected cells with an siRNA (5′-GGGAGGACCUGGAGAAGUUdTdT-3′/3′-dTdTCCCUCCUGGACCUCUUCAA-5′, obtained from Ambion) targetting both CtBP1 and CtBP2 (versus control siRNA). After 48 hours cells were either transferred to a hypoxic chamber (1% oxygen), or maintained in normoxia, for 18 hours.
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.
Project description:RNA-sequencing was performed to gain insight into the mechanism responsible for the mesenchymal-to-epithelial transition (MET) induced by loss of long non-coding RNA (lncRNA) DNM3OS in SKOV3 ovarian cancer cells. Following siRNA-mediated knockdown of DNM3OS or non-targeting control, RNA-sequencing was performed. This high-throughput data revealed knockdown of DNM3OS down-regulated the expression of genes and pathways known to induce EMT in ovarian cancer.
Project description:Acute inflammation is critical for survival, but chronic immune mediated inflammation is a leading cause for disease and mortality worldwide , while our understanding of the pathogenesis and precise treatments are still limited. Here we investigate the role of the transcriptional corepressors CTBP 1 and 2 in murine and human macrophage inflammation using loss of function models to show that CTBP2 but not CTBP1 controls inflammatory gene expression . We find that CTBP2 binds to cis-regulatory elements of inflammatory genes together with the transcription factors NFκB and AP-1 and forms a corepressor complex. Rescue of Ctbp1/2 double knockout cells with full length CTBP2 potently represses inflammatory responses while a monomeric mutant does not. Differential profiling of CTBP2’s wild type and monomeric interactome confirms oligomer-specific interactions with multiple repressors including the NuRD complex, WIZ and KDM1A. Conversely, monomers retain their ability to interact with inflammatory transcription factors and polymerase 2, boosting transcription of inflammatory genes. Our findings point to an important function for CTBP2 in the resolution of inflammation, which may contribute to the progression of inflammatory disorders and which may offer therapeutic targets in the future.
Project description:Acute inflammation is critical for survival, but chronic immune mediated inflammation is a leading cause for disease and mortality worldwide , while our understanding of the pathogenesis and precise treatments are still limited. Here we investigate the role of the transcriptional corepressors CTBP 1 and 2 in murine and human macrophage inflammation using loss of function models to show that CTBP2 but not CTBP1 controls inflammatory gene expression . We find that CTBP2 binds to cis-regulatory elements of inflammatory genes together with the transcription factors NFκB and AP-1 and forms a corepressor complex. Rescue of Ctbp1/2 double knockout cells with full length CTBP2 potently represses inflammatory responses while a monomeric mutant does not. Differential profiling of CTBP2’s wild type and monomeric interactome confirms oligomer-specific interactions with multiple repressors including the NuRD complex, WIZ and KDM1A. Conversely, monomers retain their ability to interact with inflammatory transcription factors and polymerase 2, boosting transcription of inflammatory genes. Our findings point to an important function for CTBP2 in the resolution of inflammation, which may contribute to the progression of inflammatory disorders and which may offer therapeutic targets in the future.
Project description:Gene expression profiling was carried out HeyA8 and SKOV3-ip1 ovarian cancer cell lines, treated either with vehicle control or 10 uM norepinephrine. The primary research question is whether ovarian cancer cell gene expression differs as a function of norepinephrine exposure. Gene expression profiling was carried out HeyA8 and SKOV3-ip1 ovarian cancer cell lines, treated either with vehicle control or 10 uM norepinephrine.
