Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA361568 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We analyzed the transcriptional programs regulated by PCAF and p27 in the colon cancer cell line HCT116 by ChIP-seq. PCAF or p27 knock down revealed that both regulated the expression of common genes. In this dataset, we include the expression data of 852 genes regulated by PCAF, obtained from the comparison between WT HCT116 cells and shPCAF knock down cells
2017-01-18 | GSE93694 | GEO
Project description:Purpose: WNT signaling activation in colorectal cancers (CRCs) occurs mainly through APC inactivation or, more uncommonly, β-catenin activation. Both processes promote β-catenin nuclear accumulation, which transcriptionally up-regulates epithelial-to-mesenchymal transition (EMT)-related genes. Experimental Design: We investigated β-catenin localization, downstream gene expression, and phenotypic alterations in HCT116 cells containing a wild-type (HCT116-WT) or mutant β-catenin allele (HCT116-MT), or parental cells with both WT and mutant alleles (HCT116-P). We then analyzed β-catenin localization and associated phenotypes in CRC tissues. Results: Wild-type β-catenin mainly localized at the cell membrane, whereas mutant showed predominantly nuclear localization; membranous, cytoplasmic, and nuclear localization was observed in HCT116-P cells. Microarray analysis revealed significant down-regulation of Claudin-7 and E-cadherin in HCT116-MT vs. HCT116-WT cells. Claudin-7 was also down-regulated in HCT116-P vs. HCT116-WT cells, although E-cadherin expression was unaffected. Altered expression of cell-cell junction-related molecules led to tight junction (TJ) impairment in HCT116-P, and dual loss of TJs and adherens junctions (AJs) in HCT116-MT. TJ loss increased migration and invasion activities of HCT116-WT, whereas AJ loss was required to further up-regulate these activities in HCT116-P. Immunohistochemistry analysis of 101 stage III CRC tissues revealed high nuclear β-catenin expression (≥30% of tumor cells) in 15 (14.9%) samples, low nuclear expression (1-29%) in 53 (52.5%) samples, and undetectable nuclear expression in 33 (32.6%) samples, with a trend toward more frequent down-regulation of Claudin-7 and E-cadherin, and increased metastasis in CRCs with high vs. low nuclear β-catenin. Conclusions: β-catenin activation and nuclear translocation induce EMT progression by modifying cell-cell junctions, and are associated with aggressive behaviors of CRCs.
2019-11-18 | GSE126845 | GEO
Project description:Human SV80 Cells: Control vs. Caspase-8 knock down
| PRJNA131251 | ENA
Project description:Human PC-3 prostate cancer cells: Control (shNTC non-target shRNA) vs. shETV4 knock down (shETV4)
| PRJNA147965 | ENA
Project description:rs09-07_hb6 - hb6 - The aim is to determine downstream target of HB6 transcription factor involved in plant development - Transcriptome on Arabidopsis HB6 over-expressing plants and BPM Knock down plants during development Keywords: wt vs mutant comparison
2010-08-01 | GSE19095 | GEO
Project description:We analyzed the transcriptional programs regulated by PCAF and p27 in the colon cancer cell line HCT116 by ChIP-seq. We identified 269 protein-encoding genes that contain both p27 and PCAF binding sites being the majority of these sites different for PCAF and p27
2017-06-10 | GSE93975 | GEO
Project description:Genes regulated after knock-down of Pirin in U937 cells
| PRJNA117507 | ENA
Project description:Cisplatin (CP) is a chemotherapeutic drug that is used to cure different types of cancer. CP induces DNA damage and leads to cell cycle arrest. The cyclin-dependent kinase inhibitor 1B (CDKN1B), also termed p27, plays an important role in the drug response ; and increased levels of p27 correlated with CP resistance. In HEK293 cells, we observed that p27 mRNAs levels increased whereas protein level drastically decreased in cells treated with CP; suggesting post-transcriptional regulatory events. To further understand the underlying mechanisms, we applied a biochemical approach combined with mass-spectrometry to systematically identify the RNA-binding proteins (RBPs) that are bound to the 3’UTR of p27 mRNAs in CP-treated versus non-treated cells in vivo. We found that 24 proteins, most of them known RBPs such HuR, hNRNPD, changed their association with p27 mRNA upon CP treatement. Furthermore, knock-down of a subset of the identified RBPs led to the inhibition of the CP-induced increase of p27 mRNA levels. In conclusion, these results highlight substantial rearrangement between RBPs and p27 mRNA upon CP treatment and corroborate the importance of post-transcriptional control in cellular drug response.
2019-09-27 | PXD008498 | Pride