Key result
Targeted-siRNA knockdown of TBX2 inhibits nasopharyngeal cancer cell proliferation and invasion and induces G1-phase arrest.
Why the study?
The expression and biological functions of TBX2 in nasopharyngeal cancer cells were not well understood.
TBX2 over-expression promotes nasopharyngeal cancer cell proliferation and invasion, suggesting it as a potential therapeutic target.
May support TBX2 as a therapeutic target in nasopharyngeal cancer; hypothesis-generating from animal data and requires clinical validation.
// Yan Lv 1, * , Meng Si 2, * , Nannan Chen 3, * , Ya Li 3, * , Xingkai Ma 4 , Huijun Yang 4 , Ling Zhang 1 , Hongyan Zhu 1 , Guang-yin Xu 1, 3 , Ge-ping Wu 1, 4 and C. Cao 3 1 Center of Translational Medicine, The First People Hospital of Zhangjiagang City, Soochow University, Suzhou, China 2 Department of Neurology, The Second Affiliated Hospital of Soochow University, Suzhou, China 3 Institute of Neuroscience, Soochow University, Suzhou, China 4 Department 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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Lv et al. (2017) studied Nasopharyngeal cancer. TBX2 knockdown by targeted-siRNA vs. Control was evaluated on Proliferation and invasion of NPC cells. Knockdown of TBX2 by targeted-siRNA significantly inhibited proliferation and invasion of nasopharyngeal cancer cells and induced G1-phase cell cycle arrest.
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