Salomoni P, Ferguson B J, Wyllie A H, Rich T
MRC Toxicology Unit, Lancaster Road Box 138, Leicester, LE 9HN, UK.
Cell Res. 2008 Jun;18(6):622-40. doi: 10.1038/cr.2008.58.
The PML gene is involved in the t(15;17) translocation of acute promyelocytic leukaemia (APL), which generates the oncogenic fusion protein PML (promyelocytic leukaemia protein)-retinoic acid receptor alpha. The PML protein localises to a subnuclear structure called the PML nuclear domain (PML-ND), of which PML is the essential structural component. In APL, PML-NDs are disrupted, thus implicating these structures in the pathogenesis of this leukaemia. Unexpectedly, recent studies indicate that PML and the PML-ND play a tumour suppressive role in several different types of human neoplasms in addition to APL. Because of PML's extreme versatility and involvement in multiple cellular pathways, understanding the mechanisms underlying its function, and therefore role in tumour suppression, has been a challenging task. In this review, we attempt to critically appraise the more recent advances in this field and propose new avenues of investigation.
早幼粒细胞白血病（APL）的t(15;17)易位涉及PML基因，该易位产生致癌融合蛋白早幼粒细胞白血病蛋白（PML）-维甲酸受体α。PML蛋白定位于一种称为PML核结构域（PML-ND）的亚核结构，其中PML是其必需的结构成分。在APL中，PML-ND被破坏，因此表明这些结构与这种白血病的发病机制有关。出乎意料的是，最近的研究表明，除APL外，PML和PML-ND在几种不同类型的人类肿瘤中发挥肿瘤抑制作用。由于PML具有极其多样的功能且参与多种细胞途径，了解其功能的潜在机制以及在肿瘤抑制中的作用一直是一项具有挑战性的任务。在这篇综述中，我们试图批判性地评估该领域的最新进展并提出新的研究途径。
