Nur77作为核受体超家族孤儿受体的一员,同时控制着肿瘤细胞的发生和死亡,与多种肿瘤的发生、发展存在着密切的联系。在细胞核中,Nur77作为致癌的生存因子,促进肿瘤细胞的生长;当其靶向转移到线粒体上与Bcl-2结合并改变Bcl-2的促生长表型,可以触发细胞色素C的释放,从而导致细胞凋亡。阐明Nur77从细胞核靶向转移至线粒体,绑定Bcl-2并改变其表型的机制可能意味着对于那些高度表达Bcl-2的肿瘤能找到新的治疗方法。 As a member of the nuclear receptor superfamily orphan receptor, Nur77 also controls the occurrence and death of tumor cells and is closely related to the occurrence and development of various tumors. In the nucleus, Nur77 acts as a cancer-causing survival factor that promotes the growth of tumor cells; its targeting to mitochondria to bind to Bcl-2 and alter the growth-promoting phenotype of Bcl-2 triggers cytochrome C release Lead to apoptosis. The mechanism by which Nur77 is transferred from the nucleus to the mitochondria, binds to Bcl-2 and alters its phenotype may indicate that new treatments can be found for those tumors that are highly expressed by Bcl-2.