Research Paper
microRNA-212 inhibits nasopharyngeal carcinoma progression through targeting TPD52 and inhibiting EMT and Wnt/β-catenin pathway
- 1 E.N.T. Department, PKU Care Luzhong Hospital, Tai’an, Shan Dong Province, China
- 2 E.N.T. Department, The Second Affiliated Hospital of Shandong First Medical University, Tai’an, Shan Dong Province, China
- 3 Department of Otolaryngology, Affiliated Hospital of Weifang Medical University, Weifang, Shan Dong Province, China
- 4 E.N.T. Department, People's Hospital of Huantai County, Zibo, Shan Dong Province, China
- 5 E.N.T. Department, Heze Municipal Hospital, Heze, Shan Dong Province, China
- 6 Department of Otolaryngology, Anqiu People's Hospital, Weifang, Shan Dong Province, China
Received: March 26, 2021 Accepted: August 23, 2021
https://doi.org/10.18632/aging.203764How to Cite
Copyright: © 2021 Wang 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
Purpose: The aim of this study was to investigate the role and potential mechanism of micro ribonucleic acid (miR)-212 in the development of nasopharyngeal carcinoma (NPC).
Methods: The expression levels of miR-212 and TPD52 were measured in NPC clinical tissues and cell lines by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The specific molecular mechanism was analyzed in the NPC cell line C666-1 and 6-10B with miR-212 mimic or inhibitor. The methyl thiazolyl tetrazolium (MTT) assay, wound healing and transwell migration and invasion assays were used to explore the effects of miR-212 on NPC proliferation, migration and invasion. Luciferase reporter assay was used to confirm the relationship between miR-212 and TPD52. Western blot was used to analyze the regulation of miR-212 on TPD52 protein, EMT marker proteins and Wnt/β-catenin pathways. The transplanted tumor mouse model was used to evaluate the miR-212 expression on tumor growth in vivo.
Results: MiR-212 expression was significantly decreased in NPC tissues and cell lines. Functionally, overexpression of miR-212 suppressed proliferation, migration, and invasion of NPC cells. Additionally, miR-212 was confirmed to directly target TPD52. Upregulation of TPD52 diminished the anti-cancer effect of miR-212 in NPC cells. Western blot analysis demonstrated that overexpression of miR-212 reduced the amount of marker proteins involved in the epithelial–mesenchymal transition (EMT) and the Wnt/β-catenin signaling pathway in NPC cells. Upregulation of miR-212 inhibited tumor growth in vivo.
Conclusions: MiR-212 played an inhibitory role in the progression of NPC by targeting TPD52, and inhibited the EMT and the Wnt/β-catenin signaling pathway.