Bioinformatics evaluation of targetomhas-miR-143-3p signaling pathways and related function ofHIF-1α, SNP(rs11549465) in patients with acute lymphoblastic leukemia

سال انتشار: 1399
نوع سند: مقاله کنفرانسی
زبان: انگلیسی
مشاهده: 454

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شناسه ملی سند علمی:

ICIBS01_167

تاریخ نمایه سازی: 2 آذر 1399

چکیده مقاله:

Acute lymphoblastic leukemia (ALL) is the most common cancer between children and the most frequent cause of death from cancer before 20 years of age. Leukemia can make many problems for families and society and this is a good reason for recognizing biomarkers. 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.HIF-1 functions as a master regulator of cellular and systemic homeostatic response to hypoxia by activating transcription of many genes, including those involved in energy metabolism, angiogenesis and apoptosis.This gene is a prognostic biomarker and involved in the treatment of leukemia.According to bioinformatics studies, has-miR-143-3p is predicted to target the HIF-1α gene in the angiogenesis pathway leading to cancer. And because rs11549465 is located in the coding region of the HIF-1α gene and this miRNA is exactly the same part of the gene, you are likely to target this polymorphism and thereby regulate gene expression in the cancer signaling pathway. In the present project, if according to bioinformatics predictions, the binding site of this microRNA is precisely the rs11549465 polymorphism allele and also the mutant allele, and due to the oncogenic role of HIF-1α gene and negative regulatory function of microRNAs, The expression of has-miR-143-3p is expected to decrease and consequently increase the expression of the target gene,, For this reason, it is predicted that has-miR-143-3p has less binding ability to the mutant allele (T) rs11549465 than the dominant (C) allele of this SNP and therefore the mutant allele may be dangerous and cause its gene expression to be increased and Lead cancer.

نویسندگان

Behnaz Hamzei

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

Atefeh Zamani

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

Nasrin Fatahi

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