First College of Clinical Medicine, Hebei North University, Zhangjiakou 075000, China.
First Hospital of Qinhuangdao Affiliated to Hebei North University, Qinhuangdao 066000, P.R. China.
Curr Protein Pept Sci. 2024;25(9):708-718. doi: 10.2174/0113892037292440240518194922.
Ubiquitination and deubiquitination are important mechanisms to maintain normal physiological activities, and their disorders or imbalances can lead to various diseases. As a subgroup of deubiquitinases (DUBs), the ubiquitin-specific peptidase (USP) family is closely related to many biological processes. USP53, one of the family members, is widely expressed in human tissues and participates in a variety of life activities, such as cell apoptosis, nerve transmission, and bone remodeling. Mutations in the USP53 gene can cause cholestasis and deafness and may also be a potential cause of schizophrenia. Knockout of USP53 can alleviate neuropathic pain induced by chronic constriction injury. Loss of USP53 up-regulates RANKL expression, promotes the cytogenesis and functional activity of osteoclasts, and triggers osteodestructive diseases. USP53 plays a tumor-suppressive role in lung cancer, renal clear cell carcinoma, colorectal cancer, liver cancer, and esophageal cancer but reduces the radiosensitivity of cervical cancer and esophageal cancer to induce radioresistance. Through the in-depth combination of literature and bioinformatics, this review suggested that USP53 may be a good potential biomarker or therapeutic target for diseases.
泛素化和去泛素化是维持正常生理活动的重要机制,它们的失调或失衡可导致各种疾病。作为去泛素酶 (DUB) 的一个亚群,泛素特异性肽酶 (USP) 家族与许多生物过程密切相关。USP53 是该家族的成员之一,广泛表达于人体组织中,参与多种生命活动,如细胞凋亡、神经传递和骨重塑。USP53 基因突变可导致胆汁淤积和耳聋,也可能是精神分裂症的潜在病因。USP53 的敲除可减轻慢性缩窄性损伤引起的神经病理性疼痛。USP53 的缺失可上调 RANKL 的表达,促进破骨细胞的生成和功能活性,引发骨破坏性疾病。USP53 在肺癌、肾透明细胞癌、结直肠癌、肝癌和食管癌中发挥抑癌作用,但降低了宫颈癌和食管癌的放射敏感性,从而诱导放射抵抗。通过文献和生物信息学的深入结合,本综述提示 USP53 可能是疾病的一个有潜力的良好生物标志物或治疗靶点。