USP20 activates the NF-kappaB pathway and promotes tumorigenesis in oral squamous cell carcinoma

Background: USP20 is a ubiquitin-specific protease, known to be involved in tumorigenesis, but any influence on oral squamous cell carcinoma (OSCC) or prognostic implications remain unclear. The aim of this study was to investigate the mechanism of USP20 in the progression of OSCC.Method: Bioinformatic, immunoblotting and immunohistochemical approaches were used to assess USP20 expression in OSCC. USP20 expression was correlated with OSCC clinicopathological parameters from the cancer genome atlas database. A cell model of the human tongue squamous cell carcinoma line, CAL-27, was used for USP20 knockdown experiments and the generation of a mouse xenograft model. RNA sequencing and quantitative immunoblotting was used for mechanistic studies of USP20 in OSCC pathogenesis.Results: Elevated USP20 expression was observed in OSCC tissues. USP20 knockdown impaired CAL-27 cell proliferation, invasion and migration in vitro and reduced xenograft tumor growth in vivo. USP20 knockdown also inhibited NF-kappaB signaling in CAL-27 cells, weakening the malignant phenotype.Conclusions: USP20 overexpression was associated with enhanced growth and metastasis in OSCC via an effect on NF-kappaB signaling. USP20 is a potential therapeutic target for OSCC treatment.