IMR Press / FBE / Volume 10 / Issue 1 / DOI: 10.2741/E814

Frontiers in Bioscience-Elite (FBE) is published by IMR Press from Volume 13 Issue 2 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.


RPS6KA4/MIR1237 and AURKC promoter are differentially methylated in Wilms’ tumor

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1 Instituto Nacional de Câncer Jose Alencar Gomes da Silva, Rua André Cavalcanti 37, Rio de Janeiro, Rio de Janeiro, Brazil
2 Instituto Fernandes Figueira, FIOCRUZ, Avenida Rui Barbosa 716, Rio de Janeiro, Rio de Janeiro, Brazil
3 Departamento de Genética, Instituto de Biologia, Universidade Federal do Rio de Janeiro, Cidade Universitária, 21941-901 Rio de Janeiro, Rio de Janeiro, Brazil

*Author to whom correspondence should be addressed.

Front. Biosci. (Elite Ed) 2018, 10(1), 143–154;
Published: 1 January 2018

Wilms’ tumor (WT) is the most frequent renal cancer in childhood, the occurrence of which is characterized by a relatively low frequency of associated mutations. While epigenetic alterations have been postulated to play a relevant role in the emergence of this tumor, the mechanisms involved in WT development remain largely unknown. In this study, the DNA methylation profile of WT was characterized with Beadchip array. Comparisons between WT with normal kidney identified 827 differentially methylated regions, most of which were attributable in hypermethylation in CpG islands. Among affected genes, WT1 and TP73 showed altered enhancers where hypermethylation was validaded by pyrosequencing. Thirty differentially methylated regions (DMRs) were identified in WT as compared to normal kidney, two of which were previously described. Two novel DMRs, located in RPS6KA4/MIR1237 and the AURKC promoter, were found to be hypermethylated in WT. Altogether, our data reinforced the relevance of alterations of DNA methylation in WT, highlighting the complex nature of these alterations that affect promoter regions as well as enhancers, UTRs and gene bodies.

Wilms’ tumor
DNA methylation
Differentially methylated regions
Aurora Kinase C
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