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TP53BP2: Roles in suppressing tumorigenesis and therapeutic opportunities
Genes & Diseases ( IF 6.8 ) Pub Date : 2022-09-05 , DOI: 10.1016/j.gendis.2022.08.014
Yunfei Huo 1 , Ke Cao 1 , Buxin Kou 1 , Mengyin Chai 1 , Shuangshuang Dou 1 , Dexi Chen 1 , Ying Shi 1 , Xiaoni Liu 1
Affiliation  

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.



中文翻译:

TP53BP2:在抑制肿瘤发生和治疗机会中的作用

恶性肿瘤仍然是世界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),也称为p53凋亡刺激蛋白2(ASPP2),以p53依赖性和非依赖性方式发挥着关键作用。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、HCV核心蛋白、PP1、YAP、CagA、RAS、PAR3等蛋白相互作用来调节细胞功能。此外,TP53BP2还可以通过NF-κB、RAS/MAPK、甲羟戊酸、TGF-β1、PI3K/AKT、aPKC-ι等下游信号通路调控肿瘤细胞的增殖、凋亡、自噬、迁移、EMT和耐药等。 /GLI1 和自噬途径。TP53BP2作为潜在的治疗靶点受到了越来越多的关注。我们对TP53BP2在肿瘤发生或发展中的作用以及TP53BP2涉及的信号通路进行综述,这可能为肿瘤治疗提供更深入的见解和策略。

更新日期:2022-09-05
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