Yang L, Han Y, Suarez Saiz F, Minden M D
Department of Cellular and Molecular Biology, Ontario Cancer Institute, University Health Network, Toronto, Ontario, Canada.
Leukemia. 2007 May;21(5):868-76. doi: 10.1038/sj.leu.2404624. Epub 2007 Mar 15.
The Wilms' tumor 1 (WT1) gene encodes a transcription factor important for normal cellular development and cell survival. The initial discovery of WT1 as the causative gene in an autosomal-recessive condition identified it as a tumor suppressor gene whose mutations are associated with urogenital disease and the development of kidney tumors. However, this view is not in keeping with the frequent finding of wild-type, full-length WT1 in human leukemia, breast cancer and several other cancers including the majority of Wilms' tumors. Rather, these observations suggest that in those conditions, WT1 has an oncogenic role in tumor formation. In this review, we explore the literature supporting both views of WT1 in human cancer and in particular human leukemias. To understand the mechanism by which WT1 can do this, we will also examine its functional activity as a transcription factor and the influence of protein partners on its dual behavior.
肾母细胞瘤1(WT1)基因编码一种对正常细胞发育和细胞存活至关重要的转录因子。WT1最初作为常染色体隐性疾病的致病基因被发现,这使其被确定为一种肿瘤抑制基因,其突变与泌尿生殖系统疾病和肾肿瘤的发生有关。然而,这一观点与在人类白血病、乳腺癌以及包括大多数肾母细胞瘤在内的其他几种癌症中频繁发现野生型、全长WT1的情况不符。相反,这些观察结果表明,在这些情况下,WT1在肿瘤形成中具有致癌作用。在这篇综述中,我们探讨了支持WT1在人类癌症尤其是人类白血病中这两种观点的文献。为了理解WT1能够做到这一点的机制,我们还将研究其作为转录因子的功能活性以及蛋白质伴侣对其双重行为的影响。