Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA296495 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Small interfering RNA (siRNA) mediated depletion of Lamin A/C and Lamin B2 was performed in a diploid colorectal cancer cell line - DLD1 with an aim to identify transcription deregulation across the genome.
2016-09-24 | GSE73269 | GEO
Project description:Analysis of transcriptional changes after treatment with Palbociclib, PD0325901 or combined treatment in DLD1 (colorectal cancer cell line). The aim of the study was to identify differentially regulated genes after the various treatment, particularly on the downregulated genes as these drugs are inhibitors of the CDK4/6 and MEK pathways and upon inhibition, should lead to the downregulation of pro-tumorigenic genes. Results provide important information on which transcription factors or genes that will be targeted by the inhibition of these 2 pathways
2016-11-02 | GSE74603 | GEO
Project description:We created furin KO cells in three colorectal cancer cell lines (DLD1, HCA7 and HT29) using CRISPR-Cas9 genome editing. And then we performed RNA-Seq analysis in furin KO colorectal cancer cells to identify potential effect of furin on gene expression patterns in DLD1, HCA7 and HT29 cells.
2020-03-15 | GSE130969 | GEO
Project description:To investigate the cancer properties of HERV-R knockout in the colon cancer cell line DLD1, we knocked out HERV-R from Crispr-cas9 in DLD1. We performed RNA-seq to profile gene expression in DLD1, DLD1R (HERV-R KO) cells, respectively.
2025-01-08 | GSE285815 | GEO
Project description:To investigate the function of ZNF692 in colorectal cancer, we established DLD1 cell lines in which target gene has been knocked out by CRISPR-cas. We then performed gene expression profiling analysis using data obtained from DLD1 colorectal human cells wt (sgC for guide control) or crispr knockout for ZNF692 (sgZ1 for guide 1, and sgZ3 for guide 3). We have each condition in triplicates.
2022-10-17 | GSE215838 | GEO
Project description:The nuclear lamins are extremely long-lived proteins in most cell types. As a consequence, lamin function cannot be effectively dissected with temporal precision using standard knock-down approaches. Here, we apply the auxin inducible degron (AID) system to rapidly deplete each lamin isoform within one cell cycle and reveal the immediate impacts of lamin loss on the nucleus . Surprisingly, neither acute lamin A/C (LA/C), lamin B1 (LB1), nor lamin B2 (LB2) depletion altered nuclear shape or induced nuclear blebbing, indicating that acute lamin loss is not sufficient to alter nuclear morphology. LB1 depletion is immediately followed by LA/C meshwork disorganization due to actin cytoskeletal forces on the lamina, yet neither LA/C nor LB1 depletion induced nuclear rupturing. We found that the abundant inner nuclear membrane protein LAP2β protects nuclear integrity in the absence of LB1, as depletion of both LB1 and LAP2β induced severe LA/C disorganization and frequent nuclear rupturing. Depolymerization of the actin cytoskeleton halts nuclear rupture in LAP2β- and LB1-depleted nuclei. We conclude that both LB1 and LAP2β resist cytoskeletal force to maintain regular lamin A/C meshwork organization and preserve nuclear integrity.
2025-02-17 | GSE289252 | GEO
Project description:We overexpressed YAP-S127D in DLD1 colorectal cancer cells for 21 days after sub-cutaneous (SubQ) injection into the flanks of nude mice.
2012-11-29 | GSE41508 | GEO
Project description:The series were performed to study the changes in gene expression upon diploidization of KBM7 cancer (CML) cell line. The line can exist either as a clone with 24 chromosomes (nearly haploid) or with 48 chromosomes (nearly diploid). Gene expression patterns are largely ploidy-independent, as suggested by this experiment
2014-04-10 | GSE56465 | GEO
Project description:Mesenchymal stem cells (MSC) maintain the musculoskeletal system by differentiating into multiple cell types including osteocytes and adipocytes. Mechanical signals, including strain and low intensity vibration (LIV), are important regulators of MSC differentiation. Lamin A/C is a vital nucleoskeleton protein that provides mechanical properties to the nucleus and mechanical competency to MSCs. Loss of Lamin A/C has been associated with reduced structural integrity and genomic regulation of the nucleus, but direct involvement of Lamin A/C in mechanical regulation of MSC differentiation is unknown. We investigated the effects of Lamin A/C depletion on the nucleus and regulation of adipogenesis during mechanical stimulation. Upon Lamin A/C depletion, the nucleus experienced decreased area, height, volume, and stiffness while the focal adhesion phosphorylation in response to LIV and dynamic substrate strain remained intact. Cells experiencing Lamin A/C depletion undergo slower adipogenesis than control cells indicating a loss of genomic regulation due to the depletion of Lamin A/C. Mechanical stimulation via daily LIV application induced a reduction of adiponectin protein levels in both control and Lamin A/C depleted cells. RNA-seq data indicated a large adipogenic mRNA shift in control cells while Lamin A/C depleted cells showed a blunted adipogenic mRNA profile. Treatment with LIV did not induce large trascriptome changes in ether control or Lamin A/C depleted MSCs except for lowered intereferon response, suggested that LIV effects on adipogenesis may not occur at the transcriptional level. In summary, focal adhesion activation by dynamic mechanical signals and LINC complex elements largely remain unaltered under Lamin A/C depletion. While the adipogenic commitment was dependent upon Lamin A/C, the reduction of adiponectin protein in response to LIV was independent of Lamin A/C indicating that the Lamin A/C depletion and mechanical regulation of adipogenesis may not utilize similar pathways to elicit a response in MSCs.
2020-11-15 | GSE157056 | GEO
Project description:To validate the suitability of two commonly used colorectal cancer cell lines, DLD1 and SW480, as model systems to study colorectal carcinogenesis, we treated these cell lines with beta-catenin siRNA and identified beta-catenin target genes using DNA microarrays. The list of identified target genes was compared to previously published beta-catenin target genes found in the PubMed and the GEO databases. Based on the large number of beta-catenin target genes found to be similarly regulated in DLD1, SW480 and LS174T as well as the large overlap with confirmed β-catenin target genes, we conclude that DLD1 and SW480 colon carcinoma cell lines are suitable model systems to study beta-catenin regulated genes and signaling pathways 12 arrays (2 cell lines, 2 treatments, 3 biological replicates)
2013-12-31 | E-GEOD-44097 | biostudies-arrayexpress