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Microrna Binding Site Polymorphism in Inflammatory Genes Associated With Colorectal Cancer: Literature Review and Bioinformatics Analysis Publisher Pubmed



Karimzadeh MR1 ; Zarin M2 ; Ehtesham N3 ; Khosravi S3 ; Soosanabadi M2 ; Mosallaei M3 ; Pourdavoud P4, 5
Authors
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Authors Affiliations
  1. 1. Department of medical Genetics, School of Medicine, Bam University of Medical Sciences, Bam, Iran
  2. 2. Department of medical Genetics, Semnan University of Medical Sciences, Semnan, Iran
  3. 3. Department of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
  4. 4. Iranian Red Crescent Society, Tehran, Iran
  5. 5. Azerbaijan medical university, Baku, Azerbaijan

Source: Cancer Gene Therapy Published:2020


Abstract

Inflammation, among environmental risk factors, is one of the most important contributors to colorectal cancer (CRC) development. In this way, studies revealed that the incidence of CRC in inflammatory bowel disease patients is up to 60% higher than the general population. MicroRNAs (miRNAs), small noncoding RNA molecules, have attracted excessive attention due to their fundamental role in various aspects of cellular biology, such as inflammation by binding to the 3′-untranslated regions (3′-UTR) of pro and anti-inflammatory genes. Based on multiple previous studies, SNPs at 3′-UTR can affect miRNA recognition elements by changing the thermodynamic features and secondary structure. This effect can be categorized, based on the number of changes, into four groups, including break, decrease, create, and enhance. In this paper, we will focus on functional variants in miRNA binding sites in inflammatory genes, which can modulate the risk of CRC by both investigating previous studies, regarding miRSNPs in inflammatory genes associated with CRC and recruiting in silico prediction algorithms to report putative miRSNPs in 176 inflammatory genes. In our analysis, we achieved 110 miRSNPs in 3′-UTR of 67 genes that seem good targets for future researches. © 2020, The Author(s), under exclusive licence to Springer Nature America, Inc.
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