Epigenetic alterations, along with genetic alterations, have long been regarded as the most important mechanism participating in carcinogenesis. DNA methylation, histone modifications, and RNA-mediated regulation are involved in many cellular processes that are essential to cancer initiation and progression. A plethora of chromatin-associated proteins and modifying proteins take control of these processes and they are under the modulation of signaling pathways. The phosphatidylinositol 3-kinase (PI3K)/AKT pathway (PI3K/AKT) is in manage of multiple biological processes and is frequently aberrantly activated in human cancers. Increasing evidence has demonstrated that critical epigenetic modifiers are directly or indirectly modulated by PI3K/AKT signaling, and participate in oncogenicity of PI3K cascade in cancers. In this review, we revisit the mechanism of the PI3K/AKT signaling pathway modulating epigenetic reprogramming in cancer and attempt to establish the connection between PI3K/AKT cascade and the epigenome.

长期以来，表观遗传学改变以及遗传学改变一直被认为是参与致癌作用的最重要机制。DNA甲基化，组蛋白修饰和RNA介导的调控涉及许多细胞过程，这些过程对于癌症的发生和发展至关重要。大量的染色质相关蛋白和修饰蛋白控制着这些过程，并且它们处于信号传导途径的调节之下。磷脂酰肌醇3-激酶（PI3K）/ AKT途径（PI3K / AKT）处于多种生物过程的管理中，并经常在人类癌症中异常激活。越来越多的证据表明，关键的表观遗传修饰因子被PI3K / AKT信号直接或间接调节，并参与了PI3K级联的致癌性。在这篇评论中，