Epigenetic profiling of MUTYH, KLF6, WNT1 and KLF4 genes in carcinogenesis and tumorigenesis of colorectal cancer

Autor: Babaei Kosar, Khaksar Roya, Zeinali Tahereh, Hemmati Hossein, Bandegi Ahmadreza, Samidoust Pirouz, Ashoobi Mohammad Taghi, Hashemian Hooman, Delpasand Kourosh, Talebinasab Fereshteh, Naebi Hoora, Mirpour Seyed Hossein, Keymoradzadeh Arman, Norollahi Seyedeh Elham
Jazyk: angličtina
Rok vydání: 2019
Předmět:
Zdroj: BioMedicine, Vol 9, Iss 4, p 22 (2019)
Druh dokumentu: article
ISSN: 2211-8039
DOI: 10.1051/bmdcn/2019090422
Popis: Colorectal cancer (CRC) is distinguished by epigenetic elements like DNA methylation, histone modification, histone acetylation and RNA remodeling which is related with genomic instability and tumor initiation. Correspondingly, as a main epigenetic regulation, DNA methylation has an impressive ability in order to be used in CRC targeted therapy. Meaningly, DNA methylation is identified as one of most important epigenetic regulators in gene expression and is considered as a notable potential driver in tumorigenesis and carcinogenesis through gene-silencing of tumor suppressors genes. Abnormal methylation situation, even in the level of promoter regions, does not essentially change the gene expression levels, particularly if the gene was become silenced, leaving the mechanisms of methylation without any response. According to the methylation situation which has a strong eagerness to be highly altered on CpG islands in carcinogenesis and tumorigenesis, considering its epigenetic fluctuations in finding new biomarkers is of great importance. Modifications in DNA methylation pattern and also enrichment of methylated histone signs in the promoter regions of some certain genes like MUTYH, KLF4/6 and WNT1 in different signaling pathways could be a notable key contributors to the upregulation of tumor initiation in CRC. These epigenetic alterations could be employed as a practical diagnostic biomarkers for colorectal cancer. In this review, we will be discuss these fluctuations of MUTYH, KLF4/6 and WNT1 genes in CRC.
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