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Cancer Commun (Lond). 2019 Nov 21;39(1):77. doi: 10.1186/s40880-019-0421-5.

Post-translational modification of Parkin and its research progress in cancer.

Ding D1,2, Ao X1,2, Liu Y1,2, Wang YY1,3, Fa HG1,2, Wang MY1,2, He YQ4, Wang JX5,6.

Author information

1
School of Basic Medical Sciences, Qingdao University, No. 38 Dengzhou Road, Shibei District, Qingdao, 266000, Shandong, P. R. China.
2
Center for Regenerative Medicine, Institute for Translational Medicine, College of Medicine, Qingdao University, Qingdao, 266000, Shandong, P. R. China.
3
Department of Thoracic Surgery, Affiliated Hospital of Qingdao University, Qingdao, 266000, Shandong, P. R. China.
4
Department of Gastroenterology, The Seventh Medical Center of PLA General Hospital, Beijing, 100700, China. endohe@163.com.
5
School of Basic Medical Sciences, Qingdao University, No. 38 Dengzhou Road, Shibei District, Qingdao, 266000, Shandong, P. R. China. wangjx@qdu.edu.cn.
6
Center for Regenerative Medicine, Institute for Translational Medicine, College of Medicine, Qingdao University, Qingdao, 266000, Shandong, P. R. China. wangjx@qdu.edu.cn.

Abstract

Clinical practice has shown that Parkin is the major causative gene found in an autosomal recessive juvenile parkinsonism (AR-JP) via Parkin mutations and that the Parkin protein is the core expression product of the Parkin gene, which itself belongs to an E3 ubiquitin ligase. Since the discovery of the Parkin gene in the late 1990s, researchers in many countries have begun extensive research on this gene and found that in addition to AR-JP, the Parkin gene is associated with many diseases, including type 2 diabetes, leprosy, Alzheimer's, autism, and cancer. Recent studies have found that the loss or dysfunction of Parkin has a certain relationship with tumorigenesis. In general, the Parkin gene, a well-established tumor suppressor, is deficient and mutated in a variety of malignancies. Parkin overexpression inhibits tumor cell growth and promotes apoptosis. However, the functions of Parkin in tumorigenesis and its regulatory mechanisms are still not fully understood. This article describes the structure, functions, and post-translational modifications of Parkin, and summarizes the recent advances in the tumor suppressive function of Parkin and its underlying mechanisms.

KEYWORDS:

Cancer; E3 ubiquitin ligase; NIP3-like protein X; Neddylation; Parkin; Parkin/PTEN-induced kinase 1 (PINK1); Phosphorylation; Post-translational modification; Sumoylation; Ubiquitination

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