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Research Paper|Volume 12, Issue 8|pp 7480—7490

High miR-31-5p expression promotes colon adenocarcinoma progression by targeting TNS1

Bobin Mi1, Qiushi Li2, Tong Li3, Guohui Liu1, Jiayang Sai1,3,4
  • 1Department of Orthopedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China
  • 2Department of Cardiology, Beijing Chaoyang Integrative Medicine Emergency Medical Center, Beijing 100029, China
  • 3Department of Oncology, The Third Affiliated Hospital, Beijing University of Chinese Medicine, Beijing 100029, China
  • 4Surgery Department, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115, USA
* Equal contribution
Received: December 11, 2019Accepted: March 30, 2020Published: April 21, 2020
https://doi.org/10.18632/aging.103096

Copyright © 2020 Mi et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Overexpression of the miR-31-5p contributes to tumorigenesis and metastasis in diverse neoplasms. In this study, we evaluated expression of miR-31-5p in patients with colon adenocarcinoma (COAD). We found that miR-31-5p was overexpressed in four cohorts (GSE30454, GSE41655, GSE18392, GSE108153) of COAD patients. Importantly, a LinkedOmics analysis revealed that high miR-31-5p expression was associated with poor overall survival of COAD patients. At total of 133 putative target genes of miR-31-5p were identified from TargetScan, miRDB, and TargetMiner. After integrating the target genes with 1,556 deregulated genes in COAD, 8 were acquired that may be targeted by miR-31-5p and contribute to COAD progression. Among these, tensin 1 (TNS1) showed the greatest prognostic ability in COAD and was strongly correlated with M2 macrophages, regulatory T cells, and other immune cells. These findings indicate that, in COAD, miR-31-5p is a potential prognostic factor that affects immune infiltration by targeting TNS1.