The mechanism underlying hypoxia-driven chromatin remodeling is a long-lasting question. For the last two decades, this question has been resolved in part. It is now widely agreed that hypoxia dynamically changes the methylation status of histones to control gene expression. Hypoxia-inducible factor (HIF) plays a central role in cellular responses to hypoxia through transcriptional activation of numerous genes. At least in part, the hypoxic regulation of histone methylation is attributed to the HIF-mediated expression of histone modifying enzymes. Protein hydroxylation and histone demethylation have emerged as the oxygen sensing processes because they are catalyzed by a family of 2-oxoglutarate (2OG)-dependent dioxygenases whose activities depend upon the ambient oxygen level. Recently, it has been extensively investigated that the 2OG dioxygenases oxygen-dependently regulate histone methylation. Nowadays, the hypoxic change in the histone methylation status is regarded as an important event to drive malignant behaviors of cancer cells. In this review, we introduced and summarized the cellular processes that govern hypoxia-driven regulation of histone methylation in the context of cancer biology. We also discussed the emerging roles of histone methyltransferases and demethylases in epigenetic response to hypoxia.

缺氧驱动的染色质重塑的潜在机制是一个长期存在的问题。在过去的二十年中，这个问题已得到部分解决。现已普遍认为，缺氧会动态改变组蛋白的甲基化状态，以控制基因表达。缺氧诱导因子（HIF）通过许多基因的转录激活在细胞对缺氧的反应中起着核心作用。至少部分地，组蛋白甲基化的低氧调节归因于HIF介导的组蛋白修饰酶的表达。蛋白质的羟基化和组蛋白的去甲基化已经作为氧感测过程出现了，因为它们受到2-氧戊二酸（2OG）依赖性双加氧酶家族的催化，该酶的活性取决于周围的氧气水平。最近，已经广泛地研究了2OG双加氧酶氧依赖性地调节组蛋白甲基化。如今，组蛋白甲基化状态的低氧变化被认为是驱动癌细胞恶性行为的重要事件。在这篇综述中，我们介绍并总结了在癌症生物学背景下控制缺氧驱动的组蛋白甲基化调控的细胞过程。我们还讨论了组蛋白甲基转移酶和脱甲基酶在对缺氧的表观遗传反应中的新兴作用。我们介绍并总结了在癌症生物学中控制缺氧驱动的组蛋白甲基化调控的细胞过程。我们还讨论了组蛋白甲基转移酶和脱甲基酶在对缺氧的表观遗传反应中的新兴作用。我们介绍并总结了在癌症生物学中控制缺氧驱动的组蛋白甲基化调控的细胞过程。我们还讨论了组蛋白甲基转移酶和脱甲基酶在对缺氧的表观遗传反应中的新兴作用。