Bioinformatic evaluation of the miR-3613-3p effect on TGF-beta/SMAD signaling pathway in colorectal cancer

Introduction: Colorectal cancer (CRC) is the second common cancer and the fourth major reason of cancer death in the world. Changes in the DNA inside our cells that turn on oncogenes or turn off tumor suppressor genes can cause cancers, they resulting in cells growing out of control. Accumulation of genetic changes in the epithelial cells and different intracellular signaling pathways such as TGF-beta/SMAD and WNT pathways can cause CRC. Transforming growth factor-betas (TGF-betas), play main function as tumor promoters and tumor suppressors through colorectal carcinogenesis. MicroRNAs are post-transcriptional regulators of gene expression, dysregulation of miRNAs expression has been demonstrated in most cancers. Here, the ability of miR-3613-3p (located on chromosome 13) to target TGF-beta/SMAD signaling pathways was evaluated. Methods: DIANA, Mirmap, TargetScan, and miRWalk algorithms was used to find out whether miR-3613-3p have the potential to target TGF-beta pathway key genes. Present study focused on the number of MRE in 3’-UTR region, score and conservation of seed region.Results and Discussion: Bioinformatic analysis showed miR-3613-3p might be a regulator of key genes in TGF-beta pathway including SMAD2, SMAD4, TGFBR1. It is estimated that miR-3613-3p might play important role in CRC through interaction with TGF-beta/SMAD pathway and might be considered as a new candidate for experimental evaluation for further researches.

کلیدواژه ها:

Colorectal cancer ، TGF-beta/SMAD pathway ، Bioinformatics ، MicroRNA