Huo Yunfei, Cao Ke, Kou Buxin, Chai Mengyin, Dou Shuangshuang, Chen Dexi, Shi Ying, Liu Xiaoni
Beijing Institute of Hepatology, Beijing Youan Hospital, Capital Medical University, Beijing 100069, China.
Genes Dis. 2022 Sep 5;10(5):1982-1993. doi: 10.1016/j.gendis.2022.08.014. eCollection 2023 Sep.
Malignant tumor is still a major problem worldwide. During tumorigenesis or tumor development, tumor suppressor p53-binding protein 2 (TP53BP2), also known as apoptosis stimulating protein 2 of p53 (ASPP2), plays a critical role in p53 dependent and independent manner. Expression of TP53BP2 is highly correlated with the prognosis and survival rate of malignant tumor patients. TP53BP2 can interact with p53, NF-κB p65, Bcl-2, HCV core protein, PP1, YAP, CagA, RAS, PAR3, and other proteins to regulate cell function. Moreover, TP53BP2 can also regulate the proliferation, apoptosis, autophagy, migration, EMT and drug resistance of tumor cells through downstream signaling pathways, such as NF-κB, RAS/MAPK, mevalonate, TGF-β1, PI3K/AKT, aPKC-ι/GLI1 and autophagy pathways. As a potential therapeutic target, TP53BP2 has been attracted more attention. We review the role of TP53BP2 in tumorigenesis or tumor development and the signal pathway involved in TP53BP2, which may provide more deep insight and strategies for tumor treatment.
恶性肿瘤仍然是全球范围内的一个主要问题。在肿瘤发生或肿瘤发展过程中，肿瘤抑制因子p53结合蛋白2（TP53BP2），也被称为p53凋亡刺激蛋白2（ASPP2），以p53依赖和非依赖的方式发挥关键作用。TP53BP2的表达与恶性肿瘤患者的预后和生存率高度相关。TP53BP2可以与p53、NF-κB p65、Bcl-2、丙型肝炎病毒核心蛋白、PP1、YAP、CagA、RAS、PAR3等蛋白相互作用，以调节细胞功能。此外，TP53BP2还可以通过下游信号通路，如NF-κB、RAS/MAPK、甲羟戊酸、TGF-β1、PI3K/AKT、aPKC-ι/GLI1和自噬通路，调节肿瘤细胞的增殖、凋亡、自噬、迁移、上皮-间质转化和耐药性。作为一个潜在的治疗靶点，TP53BP2已受到更多关注。我们综述了TP53BP2在肿瘤发生或肿瘤发展中的作用以及TP53BP2所涉及的信号通路，这可能为肿瘤治疗提供更深入的见解和策略。
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