1st International and 10th National Iranian Conference on Bioinformatics
Home Accepted Papers
Bioinformatics analysis of hsa-miR-135a on APC gene in patients with Familial Adenomatous Polyposis
Paper ID : 1168-ICB10
Authors:
Maryam Modrek, Irsa Alborzi, Pegah Javid, Mansoureh Azadeh *
Zist Fanavari Novin Biotechnology Department, State Technical and Vocational Training Organization, Isfahan, Iran
Abstract:
Familial Adenomatous Polyposis (FAP) is an autosomal-dominant inherited disease caused by germline mutations in the Adenomatous Polyposis Coli (APC) gene [1]. Locating on choronosome 5, the APC gene encodes a tumor suppressor protein that acts as an antagonist in Wingless-Related Integration Site (WNT) signaling pathway [2]. Defects in this gene cause FAP that usually results to malignancy [3]. The aim of our study was to find bioinformatics information about the role of APC gene in the process of FAP. For this purpose, GEO datasets was studied in order to achieve information about APC gene, miRdSNP was applied to choose microRNA involved in FAP disease. The miRBase database helped to detect data about selected microRNA. The pathways associated with APC were detected through sortment of genes in DAVID database. The information about APC gene in the carcinogene pathway was obtained from KEGG pathways. The results showed that hsa-miR-135a is predicted to target the APC gene. It targets the 3’UTR region of APC, suppresses its expression. Inactivation of the APC gene is a major initiating event in colorectal tumorigenesis. Based on the findings, it is inferred that β-catenin levels may increase due to the cessation of APC gene function. Since the WNT signaling pathway is a conserved pathway, tumorigenesis may begin because of incorrect signaling of the WNT pathway. APC-free β-catenin provokes the WNT signaling pathway as a protein, leading to active transcription of target genes. Also we saw SNP:rs6875894 (single nucleotide change c/t conversion) in nucleotide 141 on miR-135a sequence which had no effect on the emrgene of this disease.It is concluded that as APC is a tumor suppressor gene so it is not the cause of the disease and when its function is stopped by miR-135a , the cell progresses to tumorigenesis.
Keywords:
FAP; miRNA; SNP; KEGG, DAVID
Status : Paper Accepted (Poster Presentation)