Oncotarget

Research Papers:

TBX2 over-expression promotes nasopharyngeal cancer cell proliferation and invasion

Yan Lv, Meng Si, Nannan Chen, Ya Li, Xingkai Ma, Huijun Yang, Ling Zhang, Hongyan Zhu, Guang-yin Xu, Ge-ping Wu _ and C. Cao

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Oncotarget. 2017; 8:52699-52707. https://doi.org/10.18632/oncotarget.17084

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Abstract

Yan Lv1,*, Meng Si2,*, Nannan Chen3,*, Ya Li3,*, Xingkai Ma4, Huijun Yang4, Ling Zhang1, Hongyan Zhu1, Guang-yin Xu1,3, Ge-ping Wu1,4 and C. Cao3

1Center of Translational Medicine, The First People Hospital of Zhangjiagang City, Soochow University, Suzhou, China

2Department of Neurology, The Second Affiliated Hospital of Soochow University, Suzhou, China

3Institute of Neuroscience, Soochow University, Suzhou, China

4Department of Otolaryngology, The First People Hospital of Zhangjiagang City, Soochow University, Suzhou, China

*These authors have contributed equally to this work

Correspondence to:

Ge-ping Wu, email: gordon-wu@qq.com

C. Cao, email: caocong@suda.edu.cn

Guang-yin Xu, email: guangyinxu@suda.edu.cn

Keywords: TBX2, nasopharyngeal cancer, invasion, proliferation, siRNA

Received: December 06, 2016    Accepted: March 12, 2017    Published: April 13, 2017

ABSTRACT

TBX2 is a member of the T box transcription factor family. Its expression and potential biological functions in nasopharyngeal cancer (NPC) cells are studied here. We showed that TBX2 mRNA and protein expression was significantly elevated in multiple human NPC tissues, as compared with that in adjacent normal tissues. Knockdown of TBX2 by targeted-siRNA significantly inhibited proliferation and invasion of NPC cells (CNE-1 and HONE-1 lines). Meanwhile, TBX2 knockdown also induced G1-phase cell cycle arrest. At the molecular level, we discovered that expressions of several tumor suppressor genes, including p21, p27, phosphatase with tensin homology (PTEN) and E-Cadherin, were increased dramatically after TBX2 knockdown in above NPC cells. Collectively, our results imply that TBX2 over-expression promotes NPC cell proliferation and invasion, possibly via silencing several key tumor suppressor genes.


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