Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Dicer knockout induced altered miRNA profile

ABSTRACT: We detected whole genome microarray expression profiling in three pairs of Dicer knockout coloretal cell lines and their normal controls, including DLD-1, RKO and HCT116.

ORGANISM(S): Homo sapiens

PROVIDER: GSE93177 | GEO | 2017/01/06

SECONDARY ACCESSION(S): PRJNA360246

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression changes in human colorectal cell line HCT116 DICER Exon5 knockout cells

Project description:The experiment was to study the gene expression changes in human colorectal cell HCT116 DICER Exon5 knockout cells comparing to that in parental HCT116 cellls. Keywords: Cell type comparison

2007-10-26 | GSE6427 | GEO

Rnase1 responsive miRNA

Project description:To determine the importance of RNase1 on cellular miRNA function, we used a lentivirus system to stably express RNase1 in dicer wt and dicer ex5 RKO cells in serum free culture. RNase1 was found to govern miRNA that reside outside the pureview of Dicer. Assignment of RNase1 as miRNA-generating enzyme suggests that, like Dicer, RNaseA enzymes mediate essential physiological functions through regulatory RNA. Two-condition experiment, wild-type RNase1 vs mutant (6x) RNase1,in two cell lines RKO dicer wild-type and RKO dicer mutant (ex5). Biological replicates: 2 for each condition and each cell line . One replicate per array.

2015-09-15 | E-GEOD-72796 | biostudies-arrayexpress

Transcription profiling of human colorectal cell line HCT116 DICER Exon5 knockout cells

2008-06-14 | E-GEOD-6427 | biostudies-arrayexpress

Phosphoproteomic analysis of liver of Dicer knockout mice

Project description:Dicer is an essential ribonuclease involved in the biogenesis of miRNA. Previous studies have reported that Dicer is dysregulated in multiple types of cancers. To investigate the downstream phosphoproteome of Dicer, we carried out phosphotyrosine profiling of the liver of Dicer knockout of mice. We employed antibody-based enrichment of phosphotyrosine containing peptides coupled with spike-in SILAC-based quantitation. Over 400 phosphoisites were identified in each condition while 290 phosphosites were quantitated in common. Amongst these, several key signaling molecules like receptor tyrosine kinase MET, MET, PDGFR, EPHA2, EPHB4 and IGF1R/INSR were hyperphosphorylated. Also, non-receptor tyrosine kinases of Src family and their downstream effector signaling partners including IRS2 and STAT3were found to be hyperphosphorylated. Our study indicates that there is significant alteration in the signaling pathways upon ablation of Dicer.

2016-07-08 | PXD000927 | Pride

miRNA sequencing signature in acquired radioresistant and normal colorectal cancer cells.

Project description:To explore the mechanisms underlying the radioresistance of colorectal cancer, we established specifically radioresistant HCT116 cell line (HCT116-R cells) and RKO cell line (RKO-R cells) derived from HCT116 and RKO cell lines by repeatedly exposing to multi-fractionated irradiation. Then, the aberrantly expressed miRNA were detected by miRNA sequencing and their bioinformatics were analyzed.

2021-01-10 | GSE159528 | GEO

Differential miRNA expression caused by Dicer knockout in small intestine

Project description:Dicer knockout cause lipid metabolism dysregulation in small intestine. Analyses of transcriptomics and proteomics reveal key enzymes affected by Dicer knockout.

2012-01-07 | GSE34909 | GEO

Gene expression profile of Dicer knockout in mouse DP thymocytes

Project description:The RNase III enzyme dicer is essential for the processing of microRNAs (miRNAs) and small interfering RNAs (siRNAs) from double-stranded RNA precursors. miRNAs and siRNAs regulate chromatin structure, gene transcription, mRNA stability and translation in a wide range of organisms. To provide a model system to explore the role of dicer-generated RNAs in the differentiation of mammalian cells in vivo, we have generated a conditional dicer allele. Deletion of dicer at an early stage of T cell development compromised the survival of αβ lineage cells, while the numbers of γδ-expressing thymocytes were not affected. In developing thymocytes, dicer was not required for the maintenance of transcriptional silencing at pericentromeric satellite sequences (constitutive heterochromatin), the maintenance of cytosine DNA methylation and X chromosome inactivation in female cells (facultative heterochromatin) and the stable shutdown of a developmentally regulated gene (developmentally regulated gene silencing). Most remarkably, given that one-third of mammalian mRNAs are putative miRNA targets, dicer appears to be dispensable for CD4/8 lineage commitment, a process where epigenetic regulation of lineage choice has been well documented. Thus, although dicer appears critical for the development of the early embryo, it may have limited impact on the implementation of lineage-specific gene expression programs.

2015-01-28 | GSE57511 | GEO

Differential miRNA expression caused by Dicer knockout in small intestine

Project description:Dicer knockout cause lipid metabolism dysregulation in small intestine. Analyses of transcriptomics and proteomics reveal key enzymes affected by Dicer knockout. Conditional knockout of Dicer in adult mice

2012-01-07 | E-GEOD-34909 | biostudies-arrayexpress

microRNA expression signatures in colorectal cancer cell lines with demethylating treatment

Project description:To screen for epigenetically silenced miRNAs, wecarried out miRNA microarray analysis in three colorectal cancer (CRC) cell lines (HCT116, DLD-1 and RKO) treated with or without 5-aza-2'-deoxycytidine (aza). HCT116 and RKO cells were also treated with aza plus 4-phenylbutyric acid (PBA). In addition, we analyzed HCT116 cells in which the DNA methyltransferase genes DNMT1 and DNMT3B were genetically disrupted (double knockout; DKO cells), thereby abrogating DNA methylation. Expression of a majority of miRNAs was downregulated in all three CRC cell lines tested, as compared to normal colonic mucosa. DAC treatment upregulated expression of a large number of miRNAs in all three CRC cell lines, and combination treatment with DAC plus PBA induced even greater numbers of miRNAs in CRC cells. The most profound effect on the miRNA expression profile was induced by genetic disruption of DNMT1 and DNMT3B in HCT116 cells.

2011-07-01 | GSE29900 | GEO

Rnase1 responsive miRNA

2015-09-15 | GSE72796 | GEO