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MicroRNA-148b suppresses proliferation, migration, and invasion of nasopharyngeal carcinoma cells by targeting metastasis-associated gene 2

Authors Wu MH, Ye XX, Wang SC, Li QH, Lai YX, Yi YM

Received 26 February 2017

Accepted for publication 18 April 2017

Published 2 June 2017 Volume 2017:10 Pages 2815—2822


Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Ru Chen

Peer reviewer comments 2

Editor who approved publication: Dr Jianmin Xu

Minhua Wu,1,* Xiaoxia Ye,1,* Shengchun Wang,2,* Qinghua Li,3 Yinxuan Lai,4 Yanmei Yi1

Department of Histology and Embryology, Guangdong Medical University, Zhanjiang, People’s Republic of China; 2Department of Pathology, Guangdong Medical University, Dongguan, People’s Republic of China; 3Department of Hematology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, People’s Republic of China; 4Health Management and Medical Examination Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang, People’s Republic of China

*These authors contributed equally to this work

Purpose: MicroRNAs (miRNAs) play important roles in tumorigenesis and metastasis by regulating genes expression. MiRNA-148b (miR-148b) had been reported to inhibit tumor progression in some kinds of cancers, but the functions of miR-148b in nasopharyngeal carcinoma (NPC) remain largely unknown. The aim of this study was to investigate the functional role of miR-148b in NPC.
Methods: Expression of miR-148b in NPC tissues and cell lines was detected by quantitative reverse transcription polymerase chain reaction. MiR-148b was overexpressed in CNE2 and C666-1 cells by miR-148b mimic transfection. The effects of miR-148b on cell proliferation, migration, and invasion were determined by colony formation assays, cell viability assays, and transwell assays. The target gene of miR-148b was investigated by luciferase assays, and the rescue experiment was performed.
Results: MiR-148b was downregulated in NPC tissues and cell lines. Ectopic miR-148b expression significantly inhibited proliferation, migration, and invasion of CNE2 and C666-1 cells. We identified that metastasis-associated gene 2 (MTA2) is a direct target of miR-148b. Rescue experiment demonstrated that the tumor-suppressive effects of miR-148b on C666-1 cell were partly reversed by restoration of MTA2 expression. Moreover, miR-148b expression was negatively related to mRNA level of MTA2 in NPC tissues.
Conclusion: Our findings elucidate that miR-148b negatively regulates the growth, migration, and invasion of NPC cells, at least in part, by targeting MTA2. The present study indicates that miR-148b is a potential therapeutic agent for NPC.

miR-148b, metastasis-associated gene 2, proliferation, invasion, nasopharyngeal carcinoma

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