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Genomic profiles of oxidative stress-induced rat renal cell carcinomas

ABSTRACT: 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.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE36101 | GEO | 2012/08/30

SECONDARY ACCESSION(S): PRJNA152973

REPOSITORIES: GEO

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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 A/J mice

Project description:Intraperitoneal administration of ferric nitrilotriacetate initiates Fenton reaction in the renal proximal tubules in rodents. Its repeated administration ultimately leads to the development of renal cell carcinoma (RCC). We performed high-resolution microarray comparative genomic hybridization to identify characteristics in the genomic profiles of oxidative stress-induced RCCs in the mice of A/J strain.

2022-01-07 | GSE183173 | GEO

Genomic profiles of oxidative stress-induced renal cell carcinomas developed in Mutyh deficient mice

Project description:Intraperitoneal administration of ferric nitrilotriacetate initiates Fenton reaction in the renal proximal tubules in 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 RCCs and simultaneously developed malignant lymphomas in the mice. The results highlighted a substantial difference in the predisposition to chromosomal changes between animal species.

2017-10-06 | GSE99535 | GEO

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

Project description:Fenton reaction-based repeated oxidative stress via ferric nitrilotriacetate (Fe-NTA) causes renal cell carcinoma (RCC) with genetic alterations similar to those in humans. We conducted high-resolution microarray comparative genomic hybridization with Fe-NTA induced RCC obtained from both wild-type and BRCA1+/- rats to evaluate the involvement of BRCA1 haploinsufficiency in carcinogenesis.

2022-06-07 | GSE198508 | GEO

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.

2022-06-07 | GSE198507 | GEO

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

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

2007-10-01 | GSE7625 | GEO

Integrative analysis demonstrates widespread NOTCH pathway activation in patients with renal cancer and reveals aberrant DNA methylation that targets the regulatory regions of the kidney genome

Project description:Even though mutations in epigenetic regulators have been seen in renal neoplasms, their effects on the epigenome have not been elucidated. High resolution analysis of DNA methylation was performed in clear cell RCCs and matched microdissected renal tubular controls and revealed widespread hypermethylation that preferentially affected gene bodies and CpG shores. Aberrant methylation was particularly enriched in kidney specific enhancer regions associated with H3K4Me1 marks. MOTIF analysis of aberrantly methylated loci revealed enrichment for AHR, HAIRY and HIF-1 transcription factors, reflecting dysregulated hypoxia and NOTCH pathways in RCC. Parallel copy number analysis demonstrated that both genetic and epigenetic alterations led to NOTCH pathway activation in RCC. NOTCH ligands,JAGGED1 and JAGGED2, were overexpressed and associated with hypomethylation and amplification respectively in RCC samples. Examination of TCGA RNA-seq dataset revealed widespread activation of NOTCH pathway in 405 RCC samples. Samples with NOTCH pathway activation were also clinically distinct and were associated with better overall survival. Finally, transgenic expression of NOTCH1 led to dysplastic hyperproliferation of tubular epithelial cells in vivo confirming the procarcinogenic role of NOTCH. In summary, our study is the first global methylome analysis of RCC and reveals that mechanistic basis of NOTCH pathway activation in RCC. We analyzed the methylome of clear cell renal cell cancer (CCRCC) by the HELP assay. 13 cases of histologically verified CCRCC tumor samples were compared to 13 control microdissected proximal tubules from non-tumor part of nephrectomy samples

2014-07-31 | E-GEOD-49420 | biostudies-arrayexpress

Analysis of microRNA expression profiles in Xp11 renal cell carcinoma compared to normal adjacent tissue.

Project description:Renal cell carcinomas (RCCs) with Xp11 translocation (Xp11 RCC) constitute a distinctive molecular subtype characterized by chromosomal translocations involving the Xp11.2 locus, resulting in gene fusions between the TFE3 transcription factor with a second gene (usually ASPSCR1, PRCC, NONO, or SFPQ). RCCs with Xp11 translocations comprise up to 1-4% of adult cases, frequently displaying papillary architecture with epithelioid clear cells.

2017-04-27 | GSE95384 | GEO

Integrating Tumor and Healthy Epithelium in a Microphysiology Multi-compartment Approach to Study Renal Cell Carcinoma Pathophysiology

Project description:The advent of micro-physiological systems (MPS) in biomedical research has enabled the introduction of more complex and relevant physiological into in vitro models. The recreation of complex morphological features in three-dimensional environments can recapitulate otherwise absent dynamic interactions in conventional models. In this study we developed an advanced in vitro Renal Cell Carcinoma (RCC) that mimics the interplay between healthy and malignant renal tissue. Based on the TissUse Humimic platform our model combines healthy renal proximal tubule epithelial cells (RPTEC) and RCC. Co-culturing reconstructed RPTEC tubules with RCC spheroids in a closed micro-perfused circuit resulted in significant phenotypical changes to the tubules. Expression of immune factors revealed that interleukin-8 (IL-8) and tumor necrosis factor-alfa (TNF-α) were upregulated in the non-malignant cells while neutrophil gelatinase-associated lipocalin (NGAL) was downregulated in both RCC and RPTEC. Metabolic analysis revealed that RCC prompted a shift in the energy production of RPTEC tubules, inducing glycolysis, in a metabolic adaptation that likely supports RCC growth and immunogenicity. In contrast, RCC maintained stable metabolic activity, emphasizing their resilience to external factors. RNA-seq and biological process analysis of primary RTPTEC tubules demonstrated that the 3D tubular architecture and MPS conditions reverted cells to a predominant oxidative phosphorylate state, a departure from the glycolytic metabolism observed in 2D culture. This dynamic RCC co-culture model, approximates the physiology of healthy renal tubules to that of RCC, providing new insights into tumor-host interactions. Our approach can show that an RCC-MPS can expand the complexity and scope of pathophysiology and biomarker studies in kidney cancer research.

2024-05-01 | GSE244498 | GEO

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