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Analysis of the Methylation Status of CpG Sites Within Cancer-Related Genes in Equine Sarcoids Cover

Analysis of the Methylation Status of CpG Sites Within Cancer-Related Genes in Equine Sarcoids

Open Access
|Nov 2018

Abstract

In the recent years, particular attention was given to the research aimed at optimizing the use of tumour epigenetic markers. One of the best known epigenetic changes associated with the process of carcinogenesis is aberrant DNA methylation. The aim of the present research was to evaluate the methylation profile of genes potentially important in the diagnosis and/or prognosis of equine sarcoids, the most commonly detected skin tumours in Equidae. The methylation status of potential promoter sequences of nine genes: APC, CCND2, CDKN2B, DCC, RARβ, RASSF1, RASSF5, THBS1 and TRPM1, was determined using bisulfite sequencing polymerase chain reaction (BSP-CR). The results of this study did not reveal any changes in the level of DNA methylation in the analysed group of candidate genes between the tumour and healthy tissues. Despite numerous reports describing the aberrant methylation of the promoters of the analysed genes in human cancers, the data obtained did not confirm the existence of such relationships in the examined tumour tissues, which excludes the possibility of using these genes for the diagnosis of the equine sarcoid.

DOI: https://doi.org/10.2478/aoas-2018-0033 | Journal eISSN: 2300-8733 | Journal ISSN: 1642-3402
Language: English
Page range: 907 - 918
Submitted on: Mar 13, 2018
Accepted on: Jun 27, 2018
Published on: Nov 2, 2018
Published by: National Research Institute of Animal Production
In partnership with: Paradigm Publishing Services
Publication frequency: 4 issues per year

© 2018 Ewelina Semik-Gurgul, Tomek Ząbek, Agnieszka Fornal, Artur Gurgul, Klaudia Pawlina-Tyszko, Jolanta Klukowska-Rötzler, Monika Bugno-Poniewierska, published by National Research Institute of Animal Production
This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.