The role of nitric oxide in modulating the hypoxic tumor response

肿瘤细胞通过激活缺氧诱导因子1 （HIF-1）对缺氧做出反应，HIF-1控制代谢适应、血管生成和转移。来自宿主基质的入侵巨噬细胞通过释放一氧化氮与肿瘤进行交流。我们发现一氧化氮可以调节细胞的氧感应过程，控制hif -1依赖的缺氧基因激活。了解这种调节机制将有助于深入了解肿瘤与宿主之间的交流，并为靶向肿瘤细胞在缺氧条件下存活和扩散的机制提供基础。

Tumor cells respond to hypoxia by activating hypoxia-inducible factor 1 (HIF-1), which controls metabolic adaptation, angiogenesis, and metastasis. Invading macrophages from the stroma of the host communicate with the tumor by releasing nitric oxide. We have found that nitric oxide can modulate the cellular oxygen-sensing process that controls HIF-1–dependent hypoxic gene activation. Understanding the mechanisms underlying this modulation would provide a deeper insight into the communication between tumor and host and would provide the basis for targeting the mechanisms by which tumor cells survive hypoxia and spread.