Abstract
Ubiquitin C-terminal hydrolases (UCHs), a subfamily of deubiquitinating enzymes (DUBs), have been found in a variety of tumor entities and play distinct roles in the pathogenesis and development of various cancers including head and neck cancer (HNC). HNC is a heterogeneous disease arising from the mucosal epithelia of the upper aerodigestive tract, including different anatomic sites, distinct histopathologic types, as well as human papillomavirus (HPV)-positive and negative subgroups. Despite advances in multi-disciplinary treatment for HNC, the long-term survival rate of patients with HNC remains low. Emerging evidence has revealed the members of UCHs are associated with the pathogenesis and clinical prognosis of HNC, which highlights the prognostic and therapeutic implications of UCHs for patients with HNC. In this review, we summarize the physiological and pathological functions of the UCHs family, which provides enlightenment of potential mechanisms of UCHs family in HNC pathogenesis and highlights the potential consideration of UCHs as attractive drug targets.
Highlights
Head and neck cancer (HNC) represents the seventh most prevalent human malignancies with an annual incidence of 890,000 new cases worldwide, including 76,000 cases in China and 18,260 cases in Germany [1, 2]
We systematically summarize the physiological and pathological functions of the ubiquitin C-terminal hydrolases (UCHs) family in human malignancies, providing enlightenment on potential mechanisms of UCHs family in HNC pathogenesis and the potential consideration of UCHs as novel promising drug targets
Emerging evidence has revealed the members of UCHs are associated with the pathogenesis and clinical prognosis of head and neck squamous cell carcinoma (HNSCC), which highlights the prognostic and therapeutic implications of UCHs for patients with HNC
Summary
Head and neck cancer (HNC) represents the seventh most prevalent human malignancies with an annual incidence of 890,000 new cases worldwide, including 76,000 cases in China and 18,260 cases in Germany [1, 2]. Large-scale genomic profiling and proteomic studies, including The Cancer Genome Atlas (TCGA) projects, have highlighted a comprehensive molecular landscape of changes in DNA copy number, somatic mutations, promoter methylation, and protein and gene expression, indicating the critical components and signal pathway in HNSCC pathogenesis [23,24,25]. One member of UCHs family, BRCA1-associated protein-1 (BAP1), was identified to be associated with poor outcome following radiation in HPV-negative HNSCC clinical sample by proteomic and transcriptomic analysis [32].
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