An Overview of the Deubiquitinase USP53: A Promising Diagnostic Marker and Therapeutic Target

Guangce Xia, Yulin Guo, Jiajia Zhang, Meng Han, Xiangchao Meng, Ji Lv
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Abstract

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.
去泛素化酶 USP53 综述:一种前景看好的诊断标志物和治疗靶标
泛素化和去泛素化是维持正常生理活动的重要机制,它们的失调或失衡会导致各种疾病。泛素特异性肽酶(USP)家族作为去泛素化酶(DUBs)的一个亚族,与许多生物学过程密切相关。USP53 基因突变可导致胆汁淤积症和耳聋,也可能是精神分裂症的潜在病因。敲除 USP53 可减轻慢性收缩性损伤引起的神经性疼痛。USP53 缺失会上调 RANKL 的表达,促进破骨细胞的细胞生成和功能活性,诱发骨破坏性疾病。USP53 在肺癌、肾透明细胞癌、结直肠癌、肝癌和食管癌中发挥抑制肿瘤的作用,但会降低宫颈癌和食管癌的放射敏感性,从而产生放射抗性。通过文献和生物信息学的深入结合,本综述提出 USP53 可能是一个很好的潜在生物标志物或疾病治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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