ArticleJournal of cancer research and clinical oncology2023
USP2 promotes cell proliferation and metastasis in choroidal melanoma via stabilizing Snail.
Article in Journal of cancer research and clinical oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Therapeutic Potential of Targeting USP2 in Pediatric Group 3 and 4 Medulloblastomas: Insights from In Silico, Ex Vivo, and In Vitro Studies.Cerebellum (London, England) · 2026Article
- DCAF7 recruits USP2 to facilitate hepatocellular carcinoma progression by suppressing clockophagy-induced ferroptosis.Cell death & disease · 2025Article
- USP2 reversed cisplatin resistance through p53-mediated ferroptosis in NSCLC.BMC medical genomics · 2025Article
- Role of Ubiquitin-regulated EMT in Cancer Metastasis and Chemoresistance.International journal of biological sciences · 2025Review
- Control of Snail1 protein stability by post-translational modifications: the basis for a complex regulation of Snail1 function.International journal of biological sciences · 2025Review
- The role of deubiquitinase USP2 in driving bladder cancer progression by stabilizing EZH2 to epigenetically silence SOX1 expression.Translational oncology · 2024Article
- High dietary Fructose Drives Metabolic Dysfunction-Associated Steatotic Liver Disease via Activating ubiquitin-specific peptidase 2/11β-hydroxysteroid dehydrogenase type 1 Pathway in Mice.International journal of biological sciences · 2024Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundChoroidal melanoma (CM) is an intraocular tumor that arises from melanocytes. While ubiquitin-specific protease 2 (USP2) modulates the progression of numerous diseases, its role in CM is not known. This study aimed to determine the role of USP2 in CM and elucidate its molecular mechanisms.
methodsMTT, Transwell, and wound-scratch assays were used to investigate the function of USP2 in the proliferation and metastasis of CM. Western blotting and qRT-PCR were used to analyze the expression of USP2, Snail, and factors associated with the epithelial-mesenchymal transition (EMT). The relationship between USP2 and Snail was explored by co-immunoprecipitation and in vitro ubiquitination assays. A nude mouse model of CM was established for verifying the role of USP2 in vivo.
resultsUSP2 overexpression promoted proliferation and metastasis, and induced the EMT in CM cells in vitro, while specific inhibition of USP2 by ML364 produced the opposite effects. ML364 also suppressed CM tumor growth in vivo. Mechanistically, USP2 is known to deubiquitinate Snail, stabilizing the latter through the removal of its K48 poly-ubiquitin chains. However, a catalytically inactive form of USP2 (C276A) had no effect on Snail ubiquitination and failed to increase Snail protein expression. The C276A mutant was also unable to promote CM cell proliferation, migration, and invasion, as well as EMT progression. Furthermore, Snail overexpression partly counteracted the effects of ML364 on proliferation and migration, while rescuing the effects of the inhibitor on the EMT.
conclusionsThe findings demonstrated that USP2 modulated CM development through the stabilization of Snail and suggest that USP2 may be a useful target for the development of novel treatments for CM.
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