Laboratory of Veterinary Pharmacology, Joint Faculty of Veterinary Medicine, Yamaguchi University, Yamaguchi, Japan.
Genes Cells. 2023 Sep;28(9):629-641. doi: 10.1111/gtc.13057. Epub 2023 Jul 25.
SE translocation (SET) is a cancer-promoting factor whose expression is upregulated in many cancers. High SET expression positively correlates with a poor cancer prognosis. SETBP1 (SET-binding protein 1/SEB/MRD29), identified as SET-binding protein, is the causative gene of Schinzel-Giedion syndrome, which is characterized by severe intellectual disability and a distorted facial appearance. Mutations in these genetic regions are also observed in some blood cancers, such as myelodysplastic syndromes, and are associated with a poor prognosis. However, the physiological role of SETBP1 and the molecular mechanisms by which the mutations lead to disease progression have not yet been fully elucidated. In this review, we will describe the current epidemiological data on SETBP1 mutations and shed light on the current knowledge about the SET-dependent and -independent functions of SETBP1.
SE 易位(SET)是一种促进癌症的因子,其表达在许多癌症中上调。高 SET 表达与不良的癌症预后呈正相关。SETBP1(SET 结合蛋白 1/SEB/MRD29),被鉴定为 SET 结合蛋白,是 Schinzel-Giedion 综合征的致病基因,其特征为严重智力残疾和面部畸形。这些遗传区域的突变也在一些血液癌症中观察到,如骨髓增生异常综合征,并与不良预后相关。然而,SETBP1 的生理作用以及突变导致疾病进展的分子机制尚未完全阐明。在这篇综述中,我们将描述 SETBP1 突变的当前流行病学数据,并阐明当前关于 SETBP1 的 SET 依赖性和非依赖性功能的知识。