Correlation between VEGF and HIF-1α expression in human oral squamous cell carcinoma
Correlation between VEGF and HIF-1α expression in human oral squamous cell carcinoma
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DOI：
10.1016/j.yexmp.2003.10.005
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发表时间：
2004-04-01
影响因子：
3.6
通讯作者：
Messadi, DV
中科院分区：
文献类型：
--
作者：
Mohamed, KM;Le, A;Messadi, DV
了解口腔癌的发展和进展对于寻求成功的治疗干预至关重要。人口腔肿瘤体内存在的低氧微环境可能对肿瘤生长和新生血管形成有积极影响。本研究将VEGF和HIF-1 α在正常角质形成细胞和口腔癌细胞系中的表达联系起来，并确定缺氧是否在VEGF和HIF-1 α的调节中发挥作用。将三种人口腔癌细胞系和三种正常角质形成细胞暴露于常氧和缺氧培养条件。采用北方和Western印迹分析来评估VEGF和HIF-1 α在不同培养条件下的表达。进行ELISA测定以测量测试的不同细胞系中的VEGF产生。缺氧上调VEGF和HIF-1 α在正常和口腔癌细胞系中的表达，在正常和口腔癌细胞系之间具有统计学显著性差异。缺氧诱导的VEGF mRNA表达模式与HIF-1 α mRNA表达密切相关。这些结果表明，缺氧调节血管内皮生长因子和HIF-1 α在头颈癌细胞系的表达，从而建立了肿瘤缺氧和这些侵略性肿瘤的新血管生成之间的生化途径。(C)2004年爱思唯尔公司All rights reserved.
Understanding the development and progression of oral cancer is critical in the quest for successful therapeutic intervention. The hypoxic microenvironment present in human oral tumor in vivo may actively influence tumor growth and neovascularization. This study Correlates expression of both VEGF and HIF-1alpha in normal keratinocytes and oral cancer cell lines and determine whether hypoxia played a role in VEGF and HIF-1alpha regulation. Three human oral cancer cell lines and three normal keratinocytes were exposed to both normoxia and hypoxia culture conditions. Northern and Western blot analysis were used to assess VEGF and HIF-1alpha expression in the different culture conditions. ELISA assays were performed to measure VEGF production in the different cell lines tested. Hypoxia upregulated VEGF and HIF-1alpha expression on both normal and oral cancer cell lines, with a statistically significant difference between normal and oral cancer cell lines. Pattern of hypoxia-induced VEGF mRNA level tightly followed the HIF-1alpha mRNA expression in the cell lines tested. These results suggest that hypoxia regulates both VEGF and HIF-1alpha expression in head and neck carcinoma cell lines, thus establishing a biochemical pathway between tumor hypoxia and neoangiogenesis in these aggressive neoplasms. (C) 2004 Elsevier Inc. All rights reserved.