Bioinformatics evaluation of targetom has-miR-128-3p signaling pathways and related function of ALDH2, SNP (rs671) in patients withacute lymphoblastic leukemia
محل انتشار: کنگره بین المللی علوم زیست پزشکی اصفهان
سال انتشار: 1399
نوع سند: مقاله کنفرانسی
زبان: انگلیسی
مشاهده: 642
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شناسه ملی سند علمی:
ICIBS01_276
تاریخ نمایه سازی: 2 آذر 1399
چکیده مقاله:
Hematologic malignancies, account for a significant percentage of cancers in worldwide. One of the most common types of malignancies, is acute lymphoblastic leukemia (ALL). ALL is One of the major blood cancers in humans. Different genetics and environment risk factors can cause this cancer. Therefor for finding more bioinformatic information we used NCBI,miRbase, miRWALK2.0, Target scan, DAVID database and KEGG pathway.ALDH2 is the second enzyme of the major oxidative pathway of alcohol metabolism. The increased exposure to acetaldehyde in individuals with the catalytically inactive form may also confer greater susceptibility to many types of cancer. Expression of this gene is reduced in leukemia and bone marrow failure, leading to worsening leukemia.has-miR-128-3p is expected to target the ALDH2 gene in the pathway of cell proliferation that leads to leukemia. Because of the position of rs671 in the coding region of the ALDH2 gene, this microRNA is the precisely the part of the gene. It is likely to target this polymorphism.In the previous studyof has-miR-128-3p in people with acute lymphoblastic leukemia, they found that this microRNA is overexpressed and effective as an oncomiR in the development and progression of ALL.In this study, if bioinformatics predicted that the binding site of this microRNA is exactly the same as the rs671 allele and the risk allele is the mutant allele, and the expected expression of ALDH2 and the negative regulatory function of the microRNAs would be expected. has-miR-128-3p increase and then decrease the expression of its target gene. For this reason, the has-miR-128-3p is predicted to have a higher binding capacity to the rs671 mutant (A) allele than to the dominant (G) allele of this SNP and may therefore be a risky mutant allele and cause cancer.
کلیدواژه ها:
نویسندگان
Negar Bahadorzehi
Cellular-Molecular Division, Department of Biology, High Institute Nurdanesh, Meymeh, Isfahan, Iran
Massoud Houshmand
Medical Genetic Department, National Institute of Genetic Engineering and Biotechnology, Tehran, Iran
Nasrin Fattahi
Gene Raz Buali, Genetic and Biotechnology Academy, Isfahan, Iran
Atefeh Zamani
Gene Raz Buali, Genetic and Biotechnology Academy, Isfahan, Iran