Abstract
Cilia are antenna-like structures present in many vertebrate cells. These organelles detect extracellular cues, transduce signals into the cell, and play an essential role in ensuring correct cell proliferation, migration, and differentiation in a spatiotemporal manner. Not surprisingly, dysregulation of cilia can cause various diseases, including cancer and ciliopathies, which are complex disorders caused by mutations in genes regulating ciliary function. The structure and function of cilia are dynamically regulated through various mechanisms, among which E3 ubiquitin ligases and deubiquitinases play crucial roles. These enzymes regulate the degradation and stabilization of ciliary proteins through the ubiquitin–proteasome system. In this review, we briefly highlight the role of cilia in ciliopathy and cancer; describe the roles of E3 ubiquitin ligases and deubiquitinases in ciliogenesis, ciliopathy, and cancer; and highlight some of the E3 ubiquitin ligases and deubiquitinases that are potential therapeutic targets for these disorders.
Highlights
Cilia are antenna-like structures that are present in a variety of vertebrate cells [1,2,3,4,5,6]
We focus on the role of E3 ubiquitin ligases and DUBs in ciliogenesis, ciliopathy, and cancer, and suggest that these enzymes may serve as novel therapeutic targets for the development of treatments for these disorders
Because Aurora A kinase (AURKA) is associated with both cancer and ciliopathy [95,97], these findings suggest that the involvement of KCTD17 and ubiquitin-specific peptidase 8 (USP8) in cancer and ciliopathy might be mediated by effects on ciliogenesis via a TCHP–AURKA pathway
Summary
Cilia are antenna-like structures that are present in a variety of vertebrate cells [1,2,3,4,5,6]. Both motile and primary cilia contain receptors and channels that detect signals from extracellular cues, such as mechanical flow and chemical stimulation, and transduce them into the cell, where they contribute to the maintenance of proper development and homeostasis Considering these functions, it is not surprising that dysregulation of cilia function can cause cancer and other diseases, including ciliopathies, which manifest as various disease phenotypes, such as congenital anomalies, neurodevelopmental disorders, and obesity [1,6,7,8,9]. We focus on the role of E3 ubiquitin ligases and DUBs in ciliogenesis, ciliopathy, and cancer, and suggest that these enzymes may serve as novel therapeutic targets for the development of treatments for these disorders
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