低氧诱导鼻咽癌细胞表达血管内皮生长因子

背景与目的:低氧是大多数实体瘤(包括鼻咽癌)肿瘤微环境中的一个普遍存在的现象。研究表明,低氧能诱导血管内皮生长因子(vascularendothelialgrowthfactor,VEGF)在神经胶质瘤(C6)等细胞中的表达。本实验研究低氧对VEGF在体外培养的鼻咽癌细胞株(CNE-2Z)表达的影响,并探讨其与肿瘤转移的关系。方法:建立CNE-2Z细胞体外低氧细胞培养模型。在低氧处理24h后,分别以RT-PCR和Westernblot方法检测VEGF基因在mRNA和蛋白质水平的表达变化。结果:RT-PCR证实CNE-2Z细胞表达VEGF189,VEGF165,VEGF145和VEGF121等4种VEGFmRNA同工型。此四种mRNA同工型在低氧处理24h后均表达增加,分别是常氧对照组的(2.67±0.30)、(2.05±0.03)、(2.73±0.15)和(1.65±0.01)倍。Westernblot显示,低氧实验组VEGF蛋白表达是常氧对照组的(2.20±0.07)倍。结论:CNE-2Z细胞表达VEGF基因。体外低氧处理能使CNE-2Z细胞中VEGF表达增加。

Vascular endothelial growth factor gene expression in nasopharyngeal carcinoma cell line induced by hypoxia in vitro

BACKGROUND & OBJECTIVE: Hypoxia is a common phenomenon in the tumor microenvironment of most solid tumors including human nasopharyngeal neoplasms. Hypoxia can induces vascular endothelial growth factor (VEGF) gene expression in some tumor cells like glioma cell line C6. The present investigations were conducted to study the effect of hypoxia on the VEGF gene expression in cultured nasopharyngeal carcinoma (NPC) cell line CNE-2Z in vitro and to discuss its impact on tumor metastasis. METHODS: Hypoxic culture model in vitro was established to test the VEGF gene expression in CNE-2Z cell line. After cultured in the hypoxia circumstance for 24 hours, VEGF expression were tested in mRNA level and protein level by RT-PCR and Western-blot analysis, respectively. RESULTS: VEGF mRNA isoforms VEGF189, VEGF165, VEGF145,and VEGF121 were identified by RT-PCR in cultured CNE-2Z cell line. All of the four VEGF mRNA isoforms expression were increased after treated under hypoxia for 24 hours. The mRNA level of four VEGF isoforms were 2.67+/-0.30, 2.05+/-0.03, 2.73+/-0.15, and 1.65+/-0.01 folds as those in normoxic cells,respectively. Western blot analysis showed that VEGF protein expression in CNE-2Z cells was 2.20+/-0.07 folds as that in normoxic cells. CONCLUSION: VEGF gene expresses in CNE-2Z cell line and can be induced by hypoxia in vitro, this mechanism may be involve in metastasis process of NPC by inproved neoplasm angiogenesis.