《Journal of Oral and Maxillofacial Surgery》

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Promotion of Overexpressing TAZ on Proliferation, Migration, Invasion of Tongue Squamous Carcinoma and the Molecular Mechanism

LI Ao-nan1,2, GU Ke1,2, CHEN Xi-yan1,2, WANG Qi1,2, WEN Yong1,2   

  1. 1. School of Stomatology, Shandong University, Jinan 250012; 2. Shandong Provincial Key Laboratory of Oral Tissue Regeneration, Jinan 250100, Shandong Province, China
  • Online:2018-08-01 Published:2019-11-28

过表达TAZ促进口腔舌鳞癌细胞增殖迁移和侵袭的作用机制研究

李傲楠1,2, 顾 客1,2, 陈希彦1,2, 王 琪1,2, 文 勇1,2   

  1. 1. 山东大学口腔医学院种植科,山东 济南 250012;2. 山东省口腔组织再生重点实验室,山东 济南 250100
  • 通讯作者: 文 勇,副教授. E-mail: wenyong@sdu.edu.cn
  • 作者简介:李傲楠(1993—),女,山东省济宁市,硕士研究生. E-mail: 719746527@qq.com
  • 基金资助:
    国家自然基金(81300885,81402150);山东省重点研发计划(2015GSF118122,2016GSF201115,2017GSF18117);山东大学青年学者未来计划(2015WLJH53)

Abstract: Objective: To investigate the effects of overexpressing TAZ on proliferation, migration and invasion of CAL-27、SCC-15 cells and the underlying molecular mechanism. Methods: Tongue squamous carcinoma cells(CAL-27、SCC-15) were used in this study. Lentivirus packaging cells were transfected with LV5-homo-TAZ and LV5-NC, and divided cells into overexpression TAZ (OE TAZ) group and negative control (NC) group. Cell proliferation was determined using CCK-8 assays. Cell migration was measured by scracth assay and cell invasion was measured by transwell assay. The mRNA and related protein levels were detected by qRT-PCR and western blot assays. Results: Western Blot and qRT-PCR analysis revealed successful TAZ overexpression. In overexpression TAZ group, the proliferation rate increased, and cell migration and invasion increased significantly compared to NC group. Proliferation-related proteins increased, such as p-Erk and p-Akt. Epithelial-mesenchymal transition(EMT)-related protein as E-Cadherin decreased while Vimentin was increased. Conclusion: Overexpression TAZ might promote proliferation, migration and invasion by affecting the protein expressions of p-Erk、p-Akt、E-Cadherin、Vimentin in tongue squamous carcinoma CAL-27、SCC-15 cells.

Key words: TAZ, cell proliferation, cell migration, cell invasion

摘要: 目的:探究过表达Tafazzin(TAZ)对口腔舌鳞癌CAL-27、SCC-15细胞增殖迁移侵袭的影响及其作用机制。方法:利用成功过表达TAZ的慢病毒载体转染CAL-27、SCC-15细胞,分为过表达TAZ组(overexpression TAZ, OE TAZ)和对照组(negative control, NC)。用CCK-8实验检测细胞增殖;用划痕实验检测细胞的迁移;用Transwell实验检测细胞侵袭。相关基因的mRNA水平和蛋白水平分别利用实时荧光定量PCR(qRT-PCR)和Western blot检测。结果:qRT-PCR和Western blot结果显示,过表达TAZ病毒转染成功;过表达组较对照组增殖升高,迁移侵袭明显增强;增殖相关蛋白p-Erk,p-Akt表达量升高,上皮间充质转化(epithelial-mesenchymal transition,EMT)相关蛋白E-钙黏连蛋白(E-Cadherin)降低,波形蛋白(Vimentin)升高。结论:过表达TAZ可能通过影响p-Erk、p-Akt、E-Cadherin、Vimentin的表达促进口腔舌鳞癌CAL-27、SCC-15细胞的增殖迁移和侵袭。

关键词: Tafazzin(TAZ), 口腔鳞癌, 细胞增殖, 细胞迁移, 细胞侵袭

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