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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from mouse kidney epithelial cells

ABSTRACT: Fumarate hydratase (FH) is the enzyme in the Krebs cycle, which transforms fumarate to malate. Loss of fumarate hyrdragase leads to hereditary leiomyomatosis and renal cell cancer (HLRCC). The biallelic inactivation has been highly accumulated in FH-deficient cells and is considered a major pro-oncogenic factor for HLRCC tumorigenesis. We used microarrays to understand the global readaptation of cell metabolism of gene expression underlying the truncated Krebs cycle by loss of function of fumarate hydratase. The fumarate hydratase wild type and knock out cells were generated for RNA extraction and hybridization on Affymetrix microarrays.

ORGANISM(S): Mus musculus

SUBMITTER: Leon zheng

PROVIDER: E-GEOD-63438 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from mouse kidney epithelial cells

Project description:Fumarate hydratase (FH) is the enzyme in the Krebs cycle, which transforms fumarate to malate. Loss of fumarate hyrdragase leads to hereditary leiomyomatosis and renal cell cancer (HLRCC). The biallelic inactivation has been highly accumulated in FH-deficient cells and is considered a major pro-oncogenic factor for HLRCC tumorigenesis. We used microarrays to understand the global readaptation of cell metabolism of gene expression underlying the truncated Krebs cycle by loss of function of fumarate hydratase.

2014-11-19 | GSE63438 | GEO

Gene expression profile of HLRCC associated renal cell cancer

Project description:Gene expression profiles of normal kidney (3 technical replicates) and a renal tumor (3 technical replicates) from a hereditary leiomyomatosis and renal cell cancer (HLRCC) patient carrying a germline mutation in the fumarate hydratase (FH) gene.

2010-12-31 | GSE20896 | GEO

An antioxidant response phenotype is shared between hereditary and sporadic type 2 papillary renal cell carcinoma

Project description:Fumarate hydratase (FH) mutation causes hereditary type 2 papillary renal cell carcinoma (HLRCC, Hereditary Leiomyomatosis and Renal Cell Cancer (MM ID # 605839)). The main effect of FH mutation is fumarate accumulation. The current paradigm posits that the main consequence of fumarate accumulation is HIF-a stabilization. Paradoxically, FH mutation differs from other HIF-a stabilizing mutations, such as VHL and SDH mutations, in its associated tumor types. We identified that fumarate can directly up-regulate antioxidant response element (ARE)-controlled genes. We demonstrated that AKR1B10 is an ARE-controlled gene and is up-regulated upon FH knockdown as well as in FH-null cell lines. AKR1B10 overexpression is also a prominent feature in both hereditary and sporadic PRCC2. This phenotype better explains the similarities between hereditary and sporadic PRCC2. Expression profiling renal normal and tumor tissue

2011-10-17 | E-GEOD-26574 | biostudies-arrayexpress

Gene expression profile of HLRCC associated renal cell cancer

2010-12-31 | E-GEOD-20896 | biostudies-arrayexpress

Fumarate induces vesicular release of mtDNA to drive innate immunity

Project description:Fumarate Hydratase (FH) is an enzyme of the Tricarboxilic Acid Cycle (TCA) that catalyzes the conversion of fumarate into malate. In the last decade, studies have revealed FH as a bona fide tumour suppressor whose mutations cause Hereditary leiomyomatosis and renal cell carcinoma (HLRCC). Loss of FH in the kidney elicits several oncogenic signalling cascades through the accumulation of the oncometabolite fumarate. Yet, whilst the long-term consequences of FH loss have been extensively described, the acute response to FH loss has not been investigated due, in part, to the lack of a suitable model. Here, we generated a new inducible mouse model to investigate the chronology of the murine homologue of FH, Fh1, loss in the adult kidney.

2023-02-17 | GSE183745 | GEO

DPYS as a potential diagnostic biomarker in hereditary and sporadic PRCC2

Project description:Papillary renal cell carcinoma type 2 (PRCC2) is known to be very aggressive type of tumor without effictive therapy. Hereditary form of PRCC2 is caused by Fumarate Hydratase (FH) gene mutation that accompanied Hereditary Leiomyomatosis and Renal Cell Carcinoma (HLRCC) disorder. In sporadic form of PRCC2 the mutation of FH gene has not been reported. Both forms of tumors have the similar histopathological characteristics with poor survival prognosis. In this study, we profiled the gene expression of renal tumors and normal tissue from PRCC2 (hereditary and sporadic) patients in order to better understand commonalities and differences in the transcriptional landscape of PRCC2. Microarray gene expression profiling was performed on eight normal kidney tissue samples, five hereditary PRCC2 tumor tissue samples and 19 sporadic PRCC2 tumor tissue samples. Hereditary PRCC2 (HPRCC2) patients were confirmed by DNA sequencing of the FH gene.

2016-06-01 | E-GEOD-48352 | biostudies-arrayexpress

An antioxidant response phenotype is shared between hereditary and sporadic type 2 papillary renal cell carcinoma

2011-10-18 | GSE26574 | GEO

Expression data of cystic renal epithelial tissue from mice deficient for fumarate hydratase.

Project description:Fumarate hydratase (FH) mutations cause hereditary leiomyomatosis and renal cell cancer (HLRCC). We have conditionally inactivated the murine ortholog (Fh1) in renal tubular epithelial cells in order to generate an in vivo model of HLRCC. Fh1 knockout mice recapitulates important aspects of HLRCC including the development of renal cysts that overexpress hypoxia inducible factor alpha (Hifa) and Hif-target genes. We used microarrays to detail the global programme of gene expression underlying cyst development in Fh1 knockout mice and identified distinct classes of up-regulated genes during this process. Keywords: gene expression, comparison (wild-type n=3 vs knockout n=3) Renal epithelial tissue was macro-dissected from Fh1 knockout mice and sex-matched litter mate control disease-free animals for RNA extraction and hybridization on Affymetrix microarrays.

2010-12-22 | E-GEOD-10989 | biostudies-arrayexpress

Expression data of cystic renal epithelial tissue from mice deficient for fumarate hydratase.

2010-12-22 | GSE10989 | GEO

Transcription profiling of human uterine fibroids and normal myometrium

Project description:Defects in mitochondrial enzymes predispose to severe developmental defects as well as tumorigenesis. Heterozygous germline mutations in the nuclear gene encoding fumarate hydratase (FH), an enzyme catalyzing the hydration of fumarate in the Krebs tricarboxylic acid cycle, cause hereditary leiomyomatosis and renal cell cancer; yet the connection between disruption of mitochondrial metabolic pathways and neoplasia remains to be discovered. We have used an expression microarray approach for studying differences in global gene expression pattern caused by mutations in FH. Seven uterine fibroids carrying FH mutations were compared with 15 fibroids with wild-type FH. The two groups showed markedly different expression profiles, and multiple differentially expressed genes were detected. The most significant increase in FH mutants was seen in the expression of carbohydrate metabolism- and glycolysis-related genes. Other significantly up-regulated gene categories in FH mutants were, for example, iron ion homeostasis and oxidoreduction. Genes with lower expression in FH-mutant fibroids belonged to groups such as extracellular matrix, cell adhesion, muscle development and cell contraction. We show that FH mutations alter significantly the expression profiles of fibroids, most strikingly increasing the expression of genes involved in glycolysis.

2007-10-02 | E-GEOD-2724 | biostudies-arrayexpress

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