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Histone Deacetylase Inhibitors Research / Protein Degradation and Inhibitors · Journal article
Frontiers in Pharmacology · September 10, 2026
Raises a question worth testing. It does not answer one.
This is a narrative review synthesizing mechanistic and preclinical evidence on five USP family deubiquitinases (USP7, USP22, USP10, USP35, USP4) as potential cancer therapeutic targets. The article proposes that targeting these DUBs via selective inhibitors, PROTAC-mediated degradation, DUBTAC strategies, and molecular glues represents a promising approach, but acknowledges substantial challenges including substrate diversity, context-dependent function, and functional redundancy, without presenting clinical trial data to support therapeutic translation.
Narrative review.
Five USP family members (USP7, USP22, USP10, USP35, USP4) play regulatory roles in tumor-related signaling molecules including p53, PTEN, c-Myc, and PD-L1. USP family members exhibit dual regulatory roles in tumor proliferation, apoptosis resistance, metastasis, and immune evasion. Emerging therapeutic modalities include PROTAC-mediated degradation, DUBTAC-mediated tumor suppressor stabilization, and molecular glue strategies.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
This review identifies deubiquitinase inhibition as a conceptual therapeutic avenue but does not provide clinical evidence supporting implementation. Clinicians and drug developers should recognize this as a mechanistic foundation requiring translation through preclinical validation and clinical trials before clinical application.
A systematic narrative review of mechanistic literature on five deubiquitinases in cancer, proposing therapeutic targeting strategies without reporting clinical trial data or empirical evidence of efficacy.
As stated by the source record.
This review identifies deubiquitinase inhibition as a conceptual therapeutic avenue but does not provide clinical evidence supporting implementation. Clinicians and drug developers should recognize this as a mechanistic foundation requiring translation through preclinical validation and clinical trials before clinical application.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
What is missing. This record has no reported figures. That is a gap in the analysis, not a judgement about the study.
Ubiquitination is a crucial post-translational modification of proteins in eukaryotic cells. Deubiquitinating enzymes (DUBs) remove ubiquitin molecules from substrate proteins, thereby reversing ubiquitination and maintaining intracellular ubiquitin homeostasis. Dysregulation or dysfunction of DUBs is closely associated with various diseases. Among them, the ubiquitin-specific protease (USP) family, the largest subfamily of DUBs, plays a key regulatory role in tumor initiation and progression. This article systematically reviews the research progress on five representative USP family members closely linked to tumors, including USP7, USP22, USP10, USP35, and USP4, with a focus on their functional mechanisms in regulating major tumor-related signaling molecules and pathways, including p53, PTEN, c-Myc, and PD-L1. It also highlights their dual regulatory roles in tumor proliferation, resistance to apoptosis, metastasis, and immune evasion. Furthermore, this review summarizes the structural basis of USP catalysis and selectivity, the determinants of context-dependent USP functions, and the emerging roles of DUBs in tumor microenvironment remodeling and therapy resistance. We also discuss the latest advances in the development of selective inhibitors and new therapeutic modalities targeting these USPs, including PROTAC-mediated degradation, DUBTAC-mediated tumor suppressor stabilization, and molecular glue strategies. Although targeting DUBs for cancer therapy faces challenges such as substrate diversity, context-dependent functions, and functional redundancy within the family, it remains a promising strategy for tumor treatment. This review provides a theoretical foundation and research directions for further understanding the roles and mechanisms of the USP family in cancer and for developing targeted DUB-based anti-tumor therapies.
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