miR-124 suppresses proliferation and invasion of nasopharyngeal carcinoma cells through the Wnt/β-catenin signaling pathway by targeting Capn4
Authors Hu H, Wang G, Li C
Received 24 February 2017
Accepted for publication 24 April 2017
Published 23 May 2017 Volume 2017:10 Pages 2711—2720
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 2
Editor who approved publication: Prof. Dr. Jianmin Xu
Haili Hu,1,* Guanghui Wang,1,* Congying Li2
1Department of Otorhinolaryngology, Huaihe Hospital of Henan University, 2Department of Otorhinolaryngology, School of Medicine, Kaifeng University, Kaifeng, People’s Republic of China
*These authors contributed equally to this work
Background: Recent studies have demonstrated that microRNA 124 (miR-124) acts as a tumor suppressor in nasopharyngeal carcinoma (NPC); however, the exact molecular mechanism by which miR-124 exerts tumor suppression has not been well elucidated.
Materials and methods: We performed quantitative real-time PCR (qRT-PCR) to measure the expression of metastasis associated lung adenocarcinoma transcript 1, miR-124, and calpain small subunit 1 (Capn4) mRNAs in NPC cell lines. We also performed western blot analysis to detect the levels of Capn4. Furthermore, we performed MTT assay and transwell invasion assay to determine the proliferation and invasion ability of two NPC cell lines, namely, HONE1 and CNE2 cells, respectively. The verification of targets of miR-124 was performed using prediction softwares and luciferase reporter analysis.
Results: According to our results, the expression of Capn4 was found to be elevated, whereas the expression of miR-124 was lowered in NPC cell lines compared with normal nasopharyngeal cells. When we preformed overexpression of miR-124, it suppressed the proliferation and invasion of NPC cells. Moreover, miR-124 suppressed the expression of Capn4 by targeting Capn4 in HONE1 and CNE2 cells. When we preformed overexpression of Capn4, it reversed the inhibitory effect of miR-124 on the proliferation and invasion of NPC cells. Furthermore, miR-124–Capn4 axis decreased the levels of β-catenin, cyclin D1, and c-Myc, the components of the Wnt/β-catenin signaling pathway.
Conclusion: The suppression of proliferation and invasion of NPC cells by miR-124 were achieved by the regulation of Wnt/β-catenin signaling pathway by targeting Capn4. The results of this study revealed a novel miR-124–Capn4 regulatory axis in NPC cell lines, providing a better understanding of the pathogenesis of NPC and a promising therapeutic target for patients with NPC.
Keywords: miR-124, Calpain small subunit 1, NPC
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