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Transcriptome analysis of an oxidative stress-induced rat renal carcinogenesis model

ABSTRACT: An iron chelate, ferric nitrilotriacetate (Fe-NTA), induces oxidative renal tubular damage that subsequently leads to renal cell carcinoma in rodents. Here we used gene expression microarrays to find target oncogenes in this model. Network analysis of the gene expression microarray data revealed the involvement of beta-catenin pathway in the induced cancers. Keywords: dose response, disease state analysis

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE7625 | GEO | 2007/10/01

SECONDARY ACCESSION(S): PRJNA100249

REPOSITORIES: GEO

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Transcription profiling of rat renal carcinogenesis model - oxidative stress-induced

Project description:An iron chelate, ferric nitrilotriacetate (Fe-NTA), induces oxidative renal tubular damage that subsequently leads to renal cell carcinoma in rodents. Here we used gene expression microarrays to find target oncogenes in this model. Network analysis of the gene expression microarray data revealed the involvement of beta-catenin pathway in the induced cancers. Experiment Overall Design: Carcinogenesis protocol was performed using specific pathogen-free male Wistar rats or male F1 hybrid rats between Fischer344 and Brown-Norway strains. A total of 10 microarrays (Rat Genome 230 2.0; 31,999 genes; Affymetrix Inc., Santa Clara, CA) were used for the screening purpose; two for each group of untreated control, Fe-NTA treatment for 1 week, Fe-NTA treatment for 3 weeks, Fe-NTA-induced RCCs with neither peritoneal invasion nor metastasis and Fe-NTA-induced RCCs with pulmonarymetastasis.

2008-06-15 | E-GEOD-7625 | biostudies-arrayexpress

Genomic profiles of oxidative stress-induced rat renal cell carcinomas

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Genomic profiles of oxidative stress-induced rat renal cell carcinomas

Project description:Intraperitoneal administration of ferric nitrilotriacetate (Fe-NTA) initiates Fenton reaction in the renal proximal tubules of rodents that ultimately leads to a high incidence of renal cell carcinoma (RCC) after repeated treatment. We performed high-resolution microarray comparative genomic hybridization to identify characteristics in the genomic profiles of oxidative stress-induced rat RCCs. The results revealed extensive large-scale genomic alterations with a preference for deletion. Carcinogenesis protocol was performed using male F1 hybrid rats between Fischer344 and Brown-Norway strains. 13 primary tumors and 2 cell lines of Fe-NTA induced RCCs were profiled on Agilent 185K rat genome CGH microarrays. One RCC sample of a female Eker rat was also analyzed with the same Agilent 185K rat genome CGH microarray.

2012-08-30 | E-GEOD-36101 | biostudies-arrayexpress

Genomic profiles of oxidative stress-induced renal cell carcinomas developed in wild-type and BRCA1+/- SD rats

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Transcriptome analysis of subacute injured kidney by intraperitoneal injections of Fe-NTA in wildtype and BRCA1+/- rats

Project description:Fenton reaction-based repeated oxidative stress via ferric nitrilotriacetate (Fe-NTA) causes renal cell carcinoma (RCC), which was found to be promoted in BRCA1 haploinsufficiency rats.To elucidate the molecular mechanism, we performed a subacute study of repeated ip administration of Fe-NTA for 1 or 3 weeks to understand the early events. We compared the microarray gene expression profiles of rat kidney cortex tissues of wild-type and BRCA1+/- rats from the study.

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Project description:To further investigate the homeostatic response of E. faecalis to Fe exposure, we examine the whole-genome transcriptional response of wild-type (WT) exposed to non toxic Fe excess. This experiment correspond the work titled Transcriptomic response of Enterococcus faecalis to iron excess (work in preparation) A four chip study using total RNA recovered from four separate wild-type cultures of Enterococcus faecalis OG1RF, two controls samples (N medium growth) and two iron samples (N medium gowth with 0.5 mM Fe-NTA). Each chip measures the expression level of 3,114 genome genes from Enterococcus faecalis strain V583 (A7980-00-01).

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