miR-137 Regulates Proliferation, Migration, Invasion and EMT of Nasopharyngeal Carcinoma Cells by Targeting TWIST1

Author:

Fan Kaimei1,Zhu Huicheng2,Qi Lingqiang3,Huang Yingliang1,Xia Xiaoping1,Wu Kai1

Affiliation:

1. Department of Otorhinolaryngology, The First People’s Hospital of Linping District, Hangzhou, 310000, China

2. Department of Otorhinolaryngology, LinPing Hospital of Integrated Traditional Chinese and Western Medicine, Hangzhou, 310000, China

3. Department of Otorhinolaryngology, Affiliated Xiaoshan Hospital, Hangzhou Normal University, Hangzhou, 310000, China

Abstract

To investigate the effects of miR-137 on biological cell function of nasopharyngeal carcinoma (NPC) cells. Totally, 31 pairs of NPC tissues and para-cancer tissues were collected. Meanwhile, human immortalized nasopharyngeal epithelial cell lines (NP69) and human NPC cell lines (6-10B) were cultured. The abilities of cell proliferation, invasion and migration were detected by CCK-8 and Transwell assay, respectively. The relative protein and mRNA expression level was detected by Western blot and quantitative real-time polymerase chain reaction (qRT-PCR) analysis. In quantitative real-time polymerase chain reaction (qRT-PCR) experiment, miR-137 was found widely low-expressed in clinical samples and cell lines of nasopharyngeal carcinoma (NPC). On-line target gene prediction software was applied to screen potential downstream target of miR-137 in NPC. Then, Twist Family BHLH Transcription Factor 1 (TWIST1) was verified by luciferase reporter assay and Western blot experiments as a target for negative regulation of miR-137 in NPC cells. We up-regulated the expression of miR-137 and/or TWIST1 in 6-10Bin vitro, and then examined the effects of cell function after by CCK8, Transwell, scratch-wound and Western blot experiments. The results showed that decreased expression of TWIST1 resulting from up-regulation of miR-137 in 6-10B cells could inhibit the biological functions of cells including proliferation, invasion, migration and process of epithelial-mesenchymal transition (EMT). Our research discovered the suppressor function of miR-137 on NPC cells by targeting TWIST1, suggesting that miR-137 could be used as a potential therapeutic target for NPC.

Publisher

American Scientific Publishers

Subject

General Materials Science

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