Hormaeche Itsaso, Licht Jonathan D
Division of Hematology/Oncology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
Cancer Cell. 2007 Jun;11(6):475-8. doi: 10.1016/j.ccr.2007.05.005.
Oncogenic transcription factors such as PML-RARalpha, RUNX1-MTG8, and others work in large part by the recruitment of inhibitors of gene transcription to target promoters leading to aberrant repression of gene expression. PML-RARalpha, an archetypal chimeric oncoprotein, was previously shown to bring complexes of histone deacetylases (HDACs), histone methyltransferases (HMTases), and DNA methyl transferases (DNMTs) to target genes. In this issue of Cancer Cell, Villa et al. show that the full complement of chromatin machinery can be commandeered by these transcription factors with the polycomb group of proteins representing the newest identified recruit.
致癌转录因子，如早幼粒细胞白血病视黄酸受体α（PML-RARα）、核心结合因子亚单位α2-八聚体结合蛋白（RUNX1-MTG8）等，在很大程度上通过招募基因转录抑制剂至靶启动子，导致基因表达异常抑制来发挥作用。PML-RARα是一种典型的嵌合致癌蛋白，先前已表明它能将组蛋白去乙酰化酶（HDAC）、组蛋白甲基转移酶（HMTase）和DNA甲基转移酶（DNMT）复合物带到靶基因。在本期《癌细胞》杂志中，维拉等人表明，这些转录因子可以征用染色质机制的全部组成部分，其中多梳蛋白家族是最新确定的被招募对象。
