Hypoxia-inducible factors (HIFs) are transcription factors that reprogram the transcriptome for cells to survive hypoxic insults and oxidative stress. They are important during embryonic development and reprogram the cells to utilize glycolysis when the oxygen levels are extremely low. This metabolic change facilitates normal cell survival as well as cancer cell survival. The key feature in survival is the transition between acute hypoxia and chronic hypoxia, and this is regulated by the transition between HIF-1 expression and HIF-2/HIF-3 expression. This transition is observed in many human cancers and endothelial cells and referred to as the HIF Switch. Here we discuss the mechanisms involved in the HIF Switch in human endothelial and cancer cells which include mRNA and protein levels of the alpha chains of the HIFs. A major continuing effort in this field is directed towards determining the differences between normal and tumor cell utilization of this important pathway, and how this could lead to potential therapeutic approaches.

缺氧诱导因子 (HIF) 是一种转录因子，可重新编程转录组，使细胞能够在缺氧损伤和氧化应激下生存。它们在胚胎发育过程中非常重要，并在氧气水平极低时重新编程细胞以利用糖酵解。这种代谢变化有利于正常细胞的存活以及癌细胞的存活。生存的关键特征是急性缺氧和慢性缺氧之间的转变，这是由HIF-1表达和HIF-2/HIF-3表达之间的转变调节的。这种转变在许多人类癌症和内皮细胞中观察到，被称为 HIF 开关。在这里，我们讨论人内皮细胞和癌细胞中 HIF 开关的机制，包括 HIF α 链的 mRNA 和蛋白质水平。该领域的主要持续努力旨在确定正常细胞和肿瘤细胞利用这一重要途径的差异，以及这如何导致潜在的治疗方法。