An in-silico study to find potential effective circRNAs in the progression of Huntington’s disease | ||
| Iranian Journal of Basic Medical Sciences | ||
| مقاله 11، دوره 26، شماره 8، آبان 2023، صفحه 934-940 اصل مقاله (1.02 M) | ||
| نوع مقاله: Original Article | ||
| شناسه دیجیتال (DOI): 10.22038/ijbms.2023.67791.14839 | ||
| نویسندگان | ||
| Anahita Moradi1؛ Farbod Shahabinezhad1؛ Ali Dehshahri* 1، 2 | ||
| 1Pharmaceutical Sciences Research Center, Shiraz University of Medical Sciences, Shiraz, Iran | ||
| 2Department of Pharmaceutical Biotechnology, School of Pharmacy, Shiraz University of Medical Sciences, Shiraz, Iran | ||
| چکیده | ||
| Objective(s): Huntington’s disease (HD) is identified as a progressive genetic disorder caused by a mutation in the Huntington gene. Although the pathogenesis of this disease has not been fully understood, investigations have demonstrated the role of various genes and non-coding RNAs in the disease progression. In this study, we aimed to discover the potential promising circRNAs which can bind to miRNAs of HD. Materials and Methods: We used several bioinformatics tools such as ENCORI, Cytoscape, circBase, Knime, and Enrichr to collect possible circRNAs and then evaluate their connections with target miRNAs to reach this goal. We also found the probable relationship between parental genes of these circRNAs and the disease progress. Results: According to the data collected, more than 370 thousand circRNA-miRNA interactions were found for 57 target miRNAs. Several of circRNAs were spliced out of parental genes involved in the etiology of HD. Some of them need to be further investigated to elucidate their role in this neurodegenerative disease. Conclusion: This in silico investigation highlights the potential role of circRNAs in the progression of HD and opens up new horizons for drug discovery as well as diagnostic approaches for the disease. | ||
| کلیدواژهها | ||
| Bioinformatics؛ Circular RNA (circRNA)؛ Huntington’s disease؛ Micro RNA (miRNA)؛ Neurodegenerative-disorders | ||
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| مراجع | ||
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