Bioinformatics evaluation of hsa-miR-542-3p signaling pathways and its associated rs3088012 function in patients with chronic myeloid leukemia

سال انتشار: 1399
محل انتشار: کنگره بین المللی علوم زیست پزشکی اصفهان
کد COI اختصاصی: ICIBS01_033
زبان مقاله: انگلیسی
تعداد مشاهده: 474

نویسندگان

Department of Biotechnology, Faculty of Biological Science and Technology, Shahid Ashrafi Esfahani University, Isfahan, Iran

Eman Koosehlar

Department of Biotechnology, Faculty of Biological Science and Technology, University of Isfahan, Isfahan, Iran

Massoud Houshmand

Medical Genetic Department, National institute for Genetic Engineering and Biotechnology

Atefeh Zamani

Gene Raz Buali, Genetic and Biotechnology Academy, Isfahan, Iran

چکیده

Introduction & Objectives: Chronic Myeloid Leukemia (CML) is a slow-growing cancer of the blood-forming tissue. In chronic myeloid leukemia the bone marrow produces too many white blood cells. CML is characterized by the presence of the Philadelphia chromosome (Ph+), which contains the oncogenic BCR-ABL1 fusion gene resulting from a translocation between chromosomes 9 and 22. ABL1 is mutated in 8.82% of CML patients.Materials & Methods: To get more information we used NCBI, miRNASNP, miRBase, miRWALK2.0, DAVID databases and KEGG pathway as the bioinformatics tools.Results: Investigations at the rs3088012 locus indicated that T allele altered to C, which may effect on function of the miRNA associated with this region. Finally, hsa-miR-542-3p as one of the most important miRNAs related to ABL1 and given the confirmation of the role of hsa-miR-542-3p in CML through bioinformatics databases, this miRNA selected for this analysis.Conclusion: The studies due to rs3088012 have shown that when the SNP locus is in the mutant C allele, the miRNA binds to it less strongly than the wild T allele. So when this SNP occurs, hsa-miR-542-3p has less inhibitory effect on it and ABl1 is transcribed more. Due to the inhibitory action of MDM2 on p53, we predicted that a person with this harmful polymorphism is more susceptible to CML by increasing the expression of the ABL1.

کلیدواژه ها

Chronic Myeloid leukemia, hsa-miR-542-3p, CML, ABL1, KEGG pathway

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