Basic Study
Copyright ©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. May 21, 2015; 21(19): 5867-5876
Published online May 21, 2015. doi: 10.3748/wjg.v21.i19.5867
MiR-451 inhibits proliferation of esophageal carcinoma cell line EC9706 by targeting CDKN2D and MAP3K1
Guo-Qiang Zhao, Min Li, Xiao-Nan Chen, Yu-Wen Du, Yuan-Yuan Wang, Tao Wang, Xuan Yang, Wen-Qiao Zang
Wen-Qiao Zang, Xuan Yang, Yuan-Yuan Wang, Yu-Wen Du, Xiao-Nan Chen, Min Li, Guo-Qiang Zhao, College of Basic Medical Sciences, Zhengzhou University, Zhengzhou 450001, Henan Province, China
Tao Wang, Department of Hemato-tumor, the First Affiliated Hospital of Henan University of TCM, Zhengzhou 450000, Henan Province, China
Author contributions: Zhao GQ and Zang WQ designed and guided the study; Zang WQ, Yang X, Wang YY, Wang T, Li M and Du YW performed and participated in analysis of laboratory experiment data; Zang WQ and Chen XN acquired and preserved the clinical samples; Zhao GQ and Zang WQ provided administrative support and funded experiments; all authors have contributed and approved the final manuscript.
Supported by National Natural Science Foundation of China, No. 81301726.
Ethics approval: The study was approved by the Research Ethics Committee of Zhengzhou University.
Conflict-of-interest: We declare that we have no financial and personal relationships with other people or organizations that can inappropriately influence our work, and there is no professional or other personal interest of any nature or kind in any product, service and/or company that could be construed as influencing the position presented in, or the review of the manuscript.
Data sharing: No additional data are available.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Guo-Qiang Zhao, PhD, College of Basic Medical Sciences, Zhengzhou University, 100 Kexue Avenue, 450001 Zhengzhou, Henan Province, China. zhaogq@zzu.edu.cn
Telephone: +86-371-67781959
Received: December 16, 2014
Peer-review started: December 16, 2014
First decision: January 8, 2015
Revised: January 15, 2015
Accepted: February 13, 2015
Article in press: February 13, 2015
Published online: May 21, 2015
Processing time: 155 Days and 6.9 Hours
Abstract

AIM: To investigate the underlying molecular mechanisms of miR-451 to inhibit proliferation of esophageal carcinoma cell line EC9706.

METHODS: Assays for cell growth, apoptosis and invasion were used to evaluate the effects of miR-451 expression on EC cells. Luciferase reporter and Western blot assays were used to test whether cyclin-dependent kinase inhibitor 2D (CDKN2D) and MAP3K1 act as major targets of miR-451.

RESULTS: The results showed that CDKN2D and MAP3K1 are direct targets of miR-451. CDKN2D and MAP3K1 overexpression reversed the effect of miR-451. MiR-451 inhibited the proliferation of EC9706 by targeting CDKN2D and MAP3K1.

CONCLUSION: These findings suggest that miR-451 might be a novel prognostic biomarker and a potential target for the treatment of esophageal squamous cell carcinoma in the future.

Keywords: Esophageal squamous cell carcinoma; MiR-451; Cyclin-dependent kinase inhibitor 2D; MAP3K1; Proliferation

Core tip: Recently miR-451 has been reported to be tumor suppressor in human cancer cells. In the previous studies we have reported that miR-451 expression in esophageal squamous cell carcinoma (ESCC) tissues was significantly reduced, and that upregulated expression of miR-451 induced apoptosis and suppressed cell proliferation, invasion and metastasis in esophageal carcinoma. However, the underlying molecular mechanisms remain unclear. In this study, we supposed and showed that cyclin-dependent kinase inhibitor 2D (CDKN2D) and MAP3K1 are the targets of miR-451 by the bioinformatics algorithms (TargetScan and miRBase). Moreover, we found that CDKN2D and MAP3K1 contributed to ESCC malignancy.