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Clinical and biological significance of HAX-1 overexpression in nasopharyngeal carcinoma

2016; Impact Journals LLC; Volume: 7; Issue: 11 Linguagem: Inglês

10.18632/oncotarget.7274

1949-2553

Bo You, Xiaolei Cao, Xiaoyi Shao, Haosheng Ni, Si Shi, Ying Shan, Zhifeng Gu, Yiwen You,

Neutrophil, Myeloperoxidase and Oxidative Mechanisms

// Bo You 1, * , Xiaolei Cao 2, * , Xiaoyi Shao 3 , Haosheng Ni 1 , Si Shi 1 , Ying Shan 1 , Zhifeng Gu 4 , Yiwen You 1 1 Department of Otorhinolaryngology Head and Neck surgery, Affiliated Hospital of Nantong University, Nantong, Jiangsu Province, China 2 Department of Pathology, Medical School of Nantong University, Nantong, Jiangsu Province, China 3 Department of Pathogen and Immunology, Medical School of Nantong University, Nantong, Jiangsu Province, China 4 Department of Rheumatology, Affiliated Hospital of Nantong University, Nantong, Jiangsu Province, China * These authors contributed equally to this work Correspondence to: Yiwen You, e-mail: youyiwen_nantong@163.com Zhifeng Gu, e-mail: guzhifeng@126.com Keywords: exosomes, HAX-1, nasopharyngeal carcinoma, angiogenesis, prognosis Received: September 22, 2015 Accepted: January 23, 2016 Published: February 09, 2016 ABSTRACT HS1-associated protein X-1 (HAX-1) is an important marker in many types of cancers and contributes to cancer progression and metastasis. We examined the expression of HAX-1 in nasopharyngeal carcinoma (NPC) and experimentally manipulated its expression. We observed that HAX-1 expression is elevated in NPC and is correlated with lymph node metastasis, M classification, clinical stage, and poor prognosis. In addition, overexpression of HAX-1 promoted NPC proliferation both in vitro and in vivo . Exosomes are potential carriers of pro-tumorigenic factors that participate in oncogenesis. We found that NPC-derived exosomes are enriched in HAX-1 and accelerate NPC tumor growth and angiogenesis in vitro and in vivo . Furthermore, we demonstrated that oncogenic HAX-1 facilitates the growth of NPC when it is transferred via exosomes to recipient human umbilical vein endothelial cells (HUVECs). Oncogenic HAX-1 also increases the proliferation, migration, and angiogenic activity of HUVECs. Our findings provide unique insight into the pathogenesis of NPC and underscore the need to explore novel therapeutic targets such as HAX-1 to improve NPC treatment.