Guo Jun-Nan, Xia Bai-Rong, Deng Shen-Hui, Yang Chang, Pi Ya-Nan, Cui Bin-Bin, Jin Wei-Lin
Department of Colorectal Surgery, Harbin Medical University Cancer Hospital, Harbin, China.
Division of Life Sciences and Medicine, The First Affiliated Hospital of USTC, Anhui Provincial Cancer Hospital, University of Science and Technology of China, Hefei, China.
Front Cell Dev Biol. 2021 Jun 9;9:680100. doi: 10.3389/fcell.2021.680100. eCollection 2021.
Cancer stem cells (CSCs) are sparks for igniting tumor recurrence and the instigators of low response to immunotherapy and drug resistance. As one of the important components of tumor microenvironment, the tumor associated immune microenvironment (TAIM) is driving force for the heterogeneity, plasticity and evolution of CSCs. CSCs create the inhibitory TAIM (ITAIM) mainly through four stemness-related signals (SRSs), including Notch-nuclear factor-κB axis, Hedgehog, Wnt and signal transducer and activator of transcription. Ubiquitination and deubiquitination in proteins related to the specific stemness of the CSCs have a profound impact on the regulation of ITAIM. In regulating the balance between ubiquitination and deubiquitination, it is crucial for deubiquitinating enzymes (DUBs) to cleave ubiquitin chains from substrates. Ubiquitin-specific peptidases (USPs) comprise the largest family of DUBs. Growing evidence suggests that they play novel functions in contribution of ITAIM, including regulating tumor immunogenicity, activating stem cell factors, upregulating the SRSs, stabilizing anti-inflammatory receptors, and regulating anti-inflammatory cytokines. These overactive or abnormal signaling may dampen antitumor immune responses. The inhibition of USPs could play a regulatory role in SRSs and reversing ITAIM, and also have great potential in improving immune killing ability against tumor cells, including CSCs. In this review, we focus on the USPs involved in CSCs signaling pathways and regulating ITAIM, which are promising therapeutic targets in antitumor therapy.
癌症干细胞(CSCs)是引发肿瘤复发的火种,也是导致免疫治疗反应低下和耐药的诱因。作为肿瘤微环境的重要组成部分之一,肿瘤相关免疫微环境(TAIM)是CSCs异质性、可塑性和进化的驱动力。CSCs主要通过四种与干性相关的信号(SRSs)构建抑制性TAIM(ITAIM),包括Notch-核因子-κB轴、Hedgehog、Wnt以及信号转导和转录激活因子。与CSCs特定干性相关的蛋白质中的泛素化和去泛素化对ITAIM的调节具有深远影响。在调节泛素化和去泛素化之间的平衡时,去泛素化酶(DUBs)从底物上切割泛素链至关重要。泛素特异性肽酶(USPs)是DUBs中最大的家族。越来越多的证据表明,它们在ITAIM的形成中发挥新功能,包括调节肿瘤免疫原性、激活干细胞因子、上调SRSs、稳定抗炎受体以及调节抗炎细胞因子。这些过度活跃或异常的信号可能会削弱抗肿瘤免疫反应。抑制USPs可能在SRSs中发挥调节作用并逆转ITAIM,在提高对包括CSCs在内的肿瘤细胞的免疫杀伤能力方面也具有巨大潜力。在本综述中,我们重点关注参与CSCs信号通路和调节ITAIM的USPs,它们是抗肿瘤治疗中有前景的治疗靶点。