Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cells silenced for SDHB expression and tumor phenotype

ABSTRACT: Effect of SDHB silencing using siRNA methodologies in the tumor phenotype We used microarrays to detail the global programme of gene expression when SDHB is silenced. Keywords: siRNA experiment (loss of function)

ORGANISM(S): Homo sapiens

PROVIDER: GSE10289 | GEO | 2008/04/01

SECONDARY ACCESSION(S): PRJNA108499

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Cells silenced for SDHB expression and tumor phenotype

Project description:Effect of SDHB silencing using siRNA methodologies in the tumor phenotype; We used microarrays to detail the global programme of gene expression when SDHB is silenced. Experiment Overall Design: Human hepatocellular carcinoma cell line Hep3B was stably silenced with control or SDHB-specific siRNAs. <br><br>This experiment was re-loaded into ArrayExpress in November 2010 after manual curation.

2008-06-11 | E-GEOD-10289 | biostudies-arrayexpress

Gene expression in p62/SQSTM1-silenced A549 cells.

Project description:We used microarrays to detail the programme of gene expression in control or p62/SQSTM1-silenced A549 cells.

2022-07-21 | GSE208588 | GEO

A Renal CpG Island Methylator Phenotype (R-CIMP) in Kidney Tumors Associated with Germline Mutations of FH and SDHB

Project description:Germline mutations within the Krebs cycle enzyme genes fumarate hydratase (FH) or succinate dehydrogenase (SDHB, SDHC, SDHD) have been associated with an increased risk of renal cell carcinoma (RCC). These RCCs are characterized by loss of enzyme activity and significantly increased levels of intracellular fumarate or succinate that are predicted to inhibit 2-oxoglutarate-dependent dioxygenases, such as the TET enzymes that regulate DNA methylation. These tumors represent aggressive forms of RCC that can metastasize early and require specific patient management and treatment. Therefore, identifying effective and accurate methods for diagnosing these tumors is very beneficial. This study evaluated and compared the genome-wide methylation profiles of 33 RCCs from patients with RCC susceptibility syndromes, 10 associated normal samples and 13 cell-line models using the Illumina HumanMethylation450 BeadChip assay. Fifteen tumors derived from patients with germline FH (n=9) or SDHB (n=6) mutations demonstrated a distinct pattern of hypermethylation (R-CIMP) with enrichment for hypermethylation within the CpG island regions. A small, selected panel of probes was characterized that could identify R-CIMP and distinguish between FH and SDHB tumors. Cell-line models derived from HLRCC (n=3) or SDHB (n=1) kidney tumors demonstrated similar patterns of hypermethylation to the tumors, yet re-expression of either wild-type FH or SDHB did not alter the hypermethylation pattern. Treatment of the cell line models with 5-aza-2′-deoxycytidine resulted in reduced rates of invasion.

2020-10-31 | GSE126441 | GEO

SDHB gene promoter MethylTarget sequencing of normal pregnancy and recurrent spontaneous abortion patients

Project description:Our study found that low SDHB expression and high succinate levels are important for maintaining embryo implantation in the first trimester; therefore, high SDHB expression and low succinate levels during early pregnancy may increase the risk of RSA. To investigate why villous SDHB expression increases pathologically in RSA but exhibits dynamically low levels during the first trimester followed by high levels under physiological conditions, we detected CpG site methylation levels in the SDHB promoter region of villi from both individuals with RSA and controls.

2021-04-13 | GSE171877 | GEO

Expression data from TGFbeta-treated control or aPKC silenced A549 cells

2011-01-29 | GSE26241 | GEO

Genome-scale DNA methylation maps of mouse chromaffin cells with or without Sdhb knock-out.

Project description:We report the analysis of DNA methylation in mouse chromaffin cell lines using reduced representation bisulfite sequencing (RRBS). We compared DNA methylation profiles of cell lines with or without a knock-out of Sdhb gene, showing that Sdhb disruption results in a hypermethylator phenotype. Reduced representation bisulfite sequencing of 4 mouse chromaffin cell samples (2 Sdhb wild-type and 2 Sdhb knock-out).

2013-05-06 | E-GEOD-44350 | biostudies-arrayexpress

Identification of lncRNA-NTT regulated genes using small interference RNA knockdown for cDNA microarray

Project description:We used microarrays to detail the global programme of gene expression underlying lncRNA-NTT knockdown We employed small interference RNA (siRNA) and microarray techniques to investigate the effect of NTT silencing on gene expression in HepG2 cells.

2014-08-01 | GSE59957 | GEO

Genome-scale DNA methylation maps of mouse chromaffin cells with or without Sdhb knock-out.

2013-05-06 | GSE44350 | GEO

Expression data from TGFbeta-treated control or aPKC silenced A549 cells

Project description:Aberrant TGFbeta signalling is a hallmark of epithelial derived tumours. Signalling patterns can depend on the membrane trafficking and internalization of the TGFbeta receptors. Protein kinase C (PKC), particularly the atypical PKC isoforms, alter the trafficking of TGFbeta receptors and can alter TGFbeta induced gene expression. We used microarrays to detail the programme of gene expression underlying TGFbeta induction between control or aPKC silenced A549 cells. Control or aPKC silenced A549 cells were serum starved and treated with TGFbeta for 1 hour. Total RNA was extracted from untreated or TGFbeta treated cells after 8 and 24 hours and analyzed using Affymetrix microarrays. We sought to assess TGFbeta gene expression in aPKC silenced lung cancer cells, as we found that knockdown of aPKC extends TGFbeta signalling as assessed by phospho Smad2 levels. Furthermore, increased expression and oncogenic activity of aPKC (PKCiota) has been reported in lung cancer cells.

2011-01-29 | E-GEOD-26241 | biostudies-arrayexpress

The SDHB Arg230His mutation causing familial paraganglioma alters glycolysis in a new Caenorhabditis elegans model

Project description:The conserved B-subunit of succinate dehydrogenase (SDH) participates in the TCA cycle and mitochondrial electron transport. The Arg230His mutation in SDHB causes heritable pheochromocytoma/paraganglioma (PPGL). In C. elegans, we generated an in vivo PPGL model (SDHB-1 Arg244His; equivalent to human Arg230His) which manifests delayed development, shortened lifespan, attenuated ATP production and reduced mitochondrial number. Although succinate is elevated in both missense and null sdhb-1(gk165) mutants, transcriptomic comparison suggests very different causal mechanisms that are supported by metabolic analysis where only Arg244His (not null) worms elevate lactate/pyruvate levels, pointing to a missense-induced, ‘Warburg’-like aberrant glycolysis. In silico predictions of the SDHA-B dimer structure demonstrate that Arg230His modifies the catalytic cleft despite the latter’s remoteness from the mutation site. We hypothesise that Arg230His SDHB mutation rewires metabolism, reminiscent of metabolic reprogramming in cancer. Our tractable model provides a novel tool to investigate the metastatic propensity of this familial cancer and our approach may illuminate wider SDH pathology.

2020-10-01 | GSE158836 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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