缺氧对血管生成素-2在人结肠癌细胞SW480中表达的影响(2)
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参见附件。
缺氧调节Ang-2的具体机制还不是很清楚。许多人认为缺氧通过调节HIF-1途径来实现Ang-2的表达升高[6]。也有人认为缺氧是通过调节环氧化酶-2(cyclooxygenase-2，Cox-2)来实现Ang-2的表达升高。Pichiule等[7]在肝癌细胞Hepa1c4和Hepa1c1c4中研究发现Cox-2在Ang-2的缺氧诱导中起重要作用，而HIF-1在Ang-2的调节中不起作用。邢丽华等[8]研究发现在人肺腺癌A549细胞中利用Cox-2抑制剂能够抑制Ang-2的表达，呈浓度依赖性，间接说明Cox-2能够促进Ang-2的表达。具体机制还有待于进一步的研究。总之，在结肠癌细胞中，缺氧促使Ang-2表达升高。缺氧作为实体肿瘤始终存在的病理特征，必然会诱导机体产生一系列渐进性应激发应。其作为机体对缺氧应激产生的应答反应最终将能满足肿瘤加速生长的需要。
参考文献
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