// Yi Sang 1, 2, * , Ming-yuan Chen 1, * , Donghua Luo 1, * , Ru-Hua Zhang 1 , Li Wang 1 , Mei Li 1 , Rongzhen Luo 1 , Chao-Nan Qian 1 , Jian-Yong Shao 1 , Yi-Xin Zeng 1 , Tiebang Kang 1 1 State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China 2 Nanchang Key Laboratory of Cancer Pathogenesis and Translational Research, The Third Affiliated Hospital, Nanchang University, Nanchang, China * These authors have contributed equally to this work Correspondence to: Tiebang Kang, e-mail: kangtb@mail.sysu.edu.cn Keywords: nasopharyngeal carcinoma, metastasis, TEL2, SERPINE1 Received: June 02, 2015 Accepted: July 31, 2015 Published: August 13, 2015 ABSTRACT Metastasis is the major cause of treatment failure in patients with nasopharyngeal carcinoma (NPC). However, the molecular mechanisms of NPC metastasis are poorly understood. Here, using our customized gene microarray containing all of the known human transcription factors and the current markers for epithelial-mesenchymal transition, we report that TEL2 was down-regulated in highly metastatic NPC cells and the metastatic tissues in lymph node. Mechanistically, TEL2 inhibits the cell migration and invasion in vitro and metastasis in vivo by directly suppressing the SERPINE1 promoter in NPC. Consistently, an inverse correlation was observed between the protein levels of TEL2 and SERPINE1 using clinical NPC samples. Collectively, we have provided the first evidence that TEL2 plays a key role in NPC metastasis by directly down-regulating SERPINE1, and that this novel axis of TEL2 / SERPINE1 may be valuable to develop new strategies for treating NPC patients with metastasis.
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