Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Overexpression of UHRF1 drives DNA hypomethylation and hepatocellular carcinoma

ABSTRACT: UHRF1 is an essential regulator of DNA methylation that is highly expressed in many cancers. Using transgenic zebrafish, cultured cells and human tumors, we demonstrate that UHRF1 is an oncogene. RNAseq was used to assess the variation in gene expression between control and experimental samples.

ORGANISM(S): Danio rerio

PROVIDER: GSE52605 | GEO | 2013/11/22

SECONDARY ACCESSION(S): PRJNA229468

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Overexpression of UHRF1 drives DNA hypomethylation and hepatocellular carcinoma

Project description:UHRF1 is an essential regulator of DNA methylation that is highly expressed in many cancers. Using transgenic zebrafish, cultured cells and human tumors, we demonstrate that UHRF1 is an oncogene. RNAseq was used to assess the variation in gene expression between control and experimental samples. Total small RNA from 2 batches of Tg(fabp10:has.UHRF1-GFP)High and age matched Tg(fabp10:nls-mCherry) control 5 dpf zebrafish livers was purified for preparation of high-throughput sequencing libraries.

2013-11-22 | E-GEOD-52605 | biostudies-arrayexpress

UHRF1 overexpression drives DNA hypomethylation and hepatocellular carcinoma.

Project description: Not available

| S-EPMC3951208 | biostudies-literature

Gene expression profiles of uhrf1 mutant zebrafish

Project description:UHRF1 (Ubiquitin-like, containing PHD and RING finger domains, 1) recruits DNMT1 to hemimethylated DNA during replication, is essential for maintaining DNA methylation patterns during cell division and is suggested to direct additional repressive epigenetic marks. Uhrf1 mutation in zebrafish results in multiple embryonic defects including failed hepatic outgrowth, but the epigenetic basis of these phenotypes is not known. We find that DNA methylation is the only epigenetic mark that is depleted in uhrf1 mutants and make the surprising finding that despite the reduced organ size in uhrf1 mutants, genes regulating DNA replication and S-phase progression were highly upregulated. Further, there is a striking increase in BrdU incorporation in uhrf1 mutant cells, and they retained BrdU labeling over several days, indicating they are arrested in S-phase. Moreover, some of the label retaining nuclei co-localized with TUNEL positive nuclei, suggesting that arrested cells are responsible for apoptosis. Importantly, dnmt1 mutation phenocopies the S-phase arrest and hepatic outgrowth defects in uhrf1 mutants and Dnmt1 knock-down enhances the uhrf1 hepatic phenotype. Together, these data indicate that DNA hypomethylation is sufficient to generate the uhrf1 mutant phenotype by promoting an S-phase arrest. We thus propose that cell cycle arrest is a mechanism to restrict propagation of epigenetically deranged cells during embryogenesis. Genome-wide expression profiling was performed on 2 uhrf1 mutant and 2 wildtype zebrafish larvae (120 hours post fertilization) by using Zebrafish Genome Array (Affymetrix) according to manufacturer's instruction.

2015-02-09 | E-GEOD-55339 | biostudies-arrayexpress

LINE-1 hypomethylation is inversely correlated with UHRF1 overexpression in gastric cancer.

Project description: Not available

| S-EPMC5876460 | biostudies-literature

Gene expression profiles of uhrf1 mutant zebrafish

2015-02-09 | GSE55339 | GEO

DNA methylation analysis by RRBS of WT and uhrf1-hi272 mutant zebrafish whole larvae at 5 dpf

Project description:DNA methylation is a central repressive epigenetic mark. In this dataset we performed RRBS on whole zebrafish larvae from uhrf1-hi272 mutants and phenotypically wild-type siblings to determine which genomic regions have changes in DNA methylation due to uhrf1 loss.

2020-12-01 | GSE160706 | GEO

Expression data from HeLa cell lines stably expressing shRNA targeting ctrl or UHRF1

Project description:We used microarrays to explore the expression profile from cells expressing wild type and UHRF1 S674A mutant. HeLa cells expressing UHRF1 WT and S674A mutant showed similar gene expression pattern without significant affecting the transcription of DNA repari genes. UHRF1 was depleted in HeLa cells by shRNA treatment. Total RNA was purified and used to determine the global gene transcription profiles by microarray assays. The UHRF1-related genes expression profiles were compared among control cells, UHRF1-depleted cells, UHRF1 WT reconstituting cells and UHRF1 S674A mutant reconstituting cells.

2016-01-05 | E-GEOD-73751 | biostudies-arrayexpress

Comparing the genome-wide chromatin accessibility of uhrf1 hi272 mutants and phenotypically wildtype whole zebrafish embryos at 120 hpf using ATAC-Seq.

Project description:The goal of this study is to study the chromatin accessibility differences between control and uhrf1 hi272 mutant 120 hpf zebrafish embryos (uhrf1 hi272+/-, Tg(fabp10a:CAAX-EGFP) using ATAC-Seq technique.

2020-06-23 | GSE151293 | GEO

RNA sequencing of WT and Uhrf1 KO iNKT cells

Project description:Deletion of Uhrf1 resulted in stage 1-specific defects during iNKT cell development. To investigate the molecular mechanism, we sorted WT and Uhrf1-KO stage 1 iNKT cells and performed RNA-seq. By comparing gene expression profile, we found metabolic defects in Uhrf1-KO stage 1 iNKT cells. The expression of CD71 (Tfrc), two subunits of CD98 (Slc3a2 and Slc7a5) and Glut3 (Slc2a3) was reduced in stage 1 iNKT cells. Besides, the downstream pathways of AKT-mTOR axis were significantly reduced. Collectively, our results suggest that Uhrf1 is required for iNKT cell development by regulating the Akt-mTOR signaling pathway. We first sorted WT and Uhrf1-KO stage 1 iNKT cells, extracted the mRNA and performed RNA-seq. We then analyzed the differentially expressed genes and performed KEGG pathway analysis. We used RT-PCR to verify the expression of the key nutrient related genes (Tfrc, Slc3a2, Slc7a5 and Slc2a3) and used flow cytometry to test the protein level of metabolic related molecules. Besides, we also analyzed the expression of genes of mTOR downstream pathways to demonstrate that Uhrf1 mediated AKt-mTOR axis regulates iNKT cell development.

2016-03-10 | E-GEOD-77941 | biostudies-arrayexpress

Non-canonical functions of UHRF1 maintain DNA methylation homeostasis in cancer cells

Project description:DNA methylation is an essential epigenetic mark in mammals. It controls gene expression and genome stability. Global DNA methylation pattern is abnormal in cancers. Ubiquitin like with PHD and RING finger domains 1 (UHRF1) is a key epigenetic regulator that recruits and activates DNA methyltransferase 1 (DNMT1), the methylation maintenance enzyme. UHRF1 is a proven oncogene and its overexpression transforms cells in vitro and causes cancer in animal models. Therefore, UHRF1 provides a unique entry point into the links between epigenetics and cancer. However, it is still not fully clear how UHRF1 works in cancer cells. To understand UHRF1 functions in cancer, we employed experimental strategy to use an advanced chemical/genetic system, the auxin-inducible degron (AID) technology, whereby the degron-fused protein can be totally and rapidly degraded upon the addition of a small molecule, auxin. We chose the human CRC cell line HCT116 as our model and successfully generated UHRF1-AID and DNMT1-AID. Through this study, we made the significant discovery that UHRF1 not only regulates DNMT1, but also influences the activities of de novo methyltransferases DNMT3A and DNMT3B, as well as the active demethylase TET2.

2024-02-12 | GSE236026 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data