Abstract
The expression of PARK7 is upregulated in various types of cancer, suggesting its potential role as a critical regulator of the pathogenesis of cancer and in the treatment of cancer and neurodegenerative diseases, including Parkinson’s disease, Alzheimer’s disease, and Huntington disease. PARK7 activates various intracellular signaling pathways that have been implicated in the induction of tumor progression, which subsequently enhances tumor initiation, continued proliferation, metastasis, recurrence, and resistance to chemotherapy. Additionally, secreted PARK7 has been identified as a high-risk factor for the pathogenesis and survival of various cancers. This review summarizes the current understanding of the correlation between the expression of PARK7 and tumor progression.
Highlights
The human PARK7 protein, known as DJ-1, is a small ubiquitously expressed protein (20 kDa) comprising 189 amino acids
Apart from its role in neurodegenerative disorders, numerous studies have suggested that PARK7 acts as a mitogen-dependent oncogene that plays a crucial role in the progression of various types of cancer and has been identified as a novel oncoprotein involved in the Ras transduction pathway [25] (Table 1)
Consistent with its implication in various pathological processes, including Parkinson’s disease (PD), several lines of evidence indicate that the expression of PARK7 is involved in the clinicopathology of various types of cancer
Summary
The human PARK7 protein, known as DJ-1, is a small ubiquitously expressed protein (20 kDa) comprising 189 amino acids. Several mutations are involved in the pathogenesis of PD, which are being increasingly identified, and include the L166P, L10P, T19L, R26A, D149, G78G, M26I, R98Q, D149A, ∆P158, L172Q, and L172G mutations These mutations reduce the stability of PARK7 and induce loss of function. The L166P mutation leads to the loss of function of PARK7 and reduces the levels of PARK7 by inducing rapid proteolysis [15,16,17]. Deletion mutations and missense mutations of PARK7 cause loss of function by inducing the aggregation of PARK7. The mutations L10P, ∆P158, and L166P of PARK7 induce cell death by forming aggregates that impair dimerization [14]. Apart from the implication of PARK7 in the pathogenesis of PD, recent studies on PARK7 emphasize its key importance as an oncogene in the pathogenesis of cancer
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
