College of Animal Science and Technology, Northwest A&F University, Yangling Shaanxi, 712100, China.
Division of Spine, Department of Orthopedics, Tongji Hospital Affiliated to Tongji University School of Medicine, 389 Xincun Road, Shanghai, China.
Signal Transduct Target Ther. 2020 Feb 29;5(1):11. doi: 10.1038/s41392-020-0107-0.
Ubiquitination, an important type of protein posttranslational modification (PTM), plays a crucial role in controlling substrate degradation and subsequently mediates the "quantity" and "quality" of various proteins, serving to ensure cell homeostasis and guarantee life activities. The regulation of ubiquitination is multifaceted and works not only at the transcriptional and posttranslational levels (phosphorylation, acetylation, methylation, etc.) but also at the protein level (activators or repressors). When regulatory mechanisms are aberrant, the altered biological processes may subsequently induce serious human diseases, especially various types of cancer. In tumorigenesis, the altered biological processes involve tumor metabolism, the immunological tumor microenvironment (TME), cancer stem cell (CSC) stemness and so on. With regard to tumor metabolism, the ubiquitination of some key proteins such as RagA, mTOR, PTEN, AKT, c-Myc and P53 significantly regulates the activity of the mTORC1, AMPK and PTEN-AKT signaling pathways. In addition, ubiquitination in the TLR, RLR and STING-dependent signaling pathways also modulates the TME. Moreover, the ubiquitination of core stem cell regulator triplets (Nanog, Oct4 and Sox2) and members of the Wnt and Hippo-YAP signaling pathways participates in the maintenance of CSC stemness. Based on the altered components, including the proteasome, E3 ligases, E1, E2 and deubiquitinases (DUBs), many molecular targeted drugs have been developed to combat cancer. Among them, small molecule inhibitors targeting the proteasome, such as bortezomib, carfilzomib, oprozomib and ixazomib, have achieved tangible success. In addition, MLN7243 and MLN4924 (targeting the E1 enzyme), Leucettamol A and CC0651 (targeting the E2 enzyme), nutlin and MI-219 (targeting the E3 enzyme), and compounds G5 and F6 (targeting DUB activity) have also shown potential in preclinical cancer treatment. In this review, we summarize the latest progress in understanding the substrates for ubiquitination and their special functions in tumor metabolism regulation, TME modulation and CSC stemness maintenance. Moreover, potential therapeutic targets for cancer are reviewed, as are the therapeutic effects of targeted drugs.
泛素化是一种重要的蛋白质翻译后修饰(PTM)类型,在控制底物降解中发挥关键作用,进而调节各种蛋白质的“数量”和“质量”,以确保细胞内环境稳定并保证生命活动。泛素化的调控具有多面性,不仅在转录和翻译后水平(磷酸化、乙酰化、甲基化等)发挥作用,而且在蛋白质水平(激活剂或抑制剂)发挥作用。当调控机制发生异常时,改变的生物学过程可能随后导致严重的人类疾病,尤其是各种类型的癌症。在肿瘤发生过程中,改变的生物学过程涉及肿瘤代谢、免疫肿瘤微环境(TME)、癌症干细胞(CSC)干性等。在肿瘤代谢方面,RagA、mTOR、PTEN、AKT、c-Myc 和 P53 等一些关键蛋白的泛素化显著调节 mTORC1、AMPK 和 PTEN-AKT 信号通路的活性。此外,TLR、RLR 和 STING 依赖性信号通路中的泛素化也调节 TME。此外,核心干细胞调节三联体(Nanog、Oct4 和 Sox2)和 Wnt 和 Hippo-YAP 信号通路成员的泛素化参与 CSC 干性的维持。基于改变的成分,包括蛋白酶体、E3 连接酶、E1、E2 和去泛素化酶(DUBs),已经开发出许多分子靶向药物来对抗癌症。其中,针对蛋白酶体的小分子抑制剂,如硼替佐米、卡非佐米、奥普佐米和伊沙佐米,已取得显著成效。此外,MLN7243 和 MLN4924(针对 E1 酶)、Leucettamol A 和 CC0651(针对 E2 酶)、nutlin 和 MI-219(针对 E3 酶)以及化合物 G5 和 F6(针对 DUB 活性)在癌症的临床前治疗中也显示出潜力。在本综述中,我们总结了在理解泛素化底物及其在肿瘤代谢调控、TME 调节和 CSC 干性维持中的特殊功能方面的最新进展。此外,还综述了癌症的潜在治疗靶点和靶向药物的治疗效果。