ArticleOncogene2025
USP5 deubiquitinates and stabilizes IMPDH2, to promote hepatocellular carcinoma progression.
Article in Oncogene, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- MMF inhibits poxvirus infection by disrupting IMPDH2 interaction with USP5 and inducing its rod-and-ring assemblies.Virologica Sinica · 2026Article
- USP5 in cancer: a therapeutic window into metabolism and drug resistance.Journal of translational medicine · 2026Review
- USP5 inhibition stimulates immunogenic ferroptosis that enhances immunotherapy in diffuse large B-cell lymphoma.Cell communication and signaling : CCS · 2026Article
- USP5 promotes glycolysis in cervical cancer by stabilizing FOXM1.American journal of cancer research · 2026Article
- LC3-dependent intercellular transfer of phosphorylated STAT1/2 elicits CXCL9+ macrophages and enhances radiation-induced antitumor immunity.The Journal of clinical investigation · 2025Article
- Stabilization of FASN by USP5-mediated deubiquitination promotes hepatocellular carcinoma progression.Oncogenesis · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Modulating deubiquitinase activity is an emerging therapeutic approach for cancer. In this study, ubiquitin-specific protease 5 (USP5), a deubiquitinase, was found to be frequently overexpressed in hepatocellular carcinoma (HCC) and associated with poor prognosis in patients with HCC. Inosine monophosphate dehydrogenase 2 (IMPDH2) was identified as a binding partner of USP5. USP5 N-terminal domain (cryptic ZnF-UBP and ZnF-UBP domain) interacted with IMPDH2 (251-514 aa). IMPDH2 positively correlated with USP5 expression in HCC. Mechanistically, USP5 removed Lys48-linked ubiquitin chains from IMPDH2 through its deubiquitinase activity, preventing its ubiquitin-mediated degradation and stabilizing IMPDH2. The USP5-IMPDH2 axis promoted HCC proliferation, and metastasis mediated by epithelial-mesenchymal transition (EMT) process in HCC cells and Huh7 xenograft tumors in zebrafish. Notably, GTP biosynthesis pathway was involved in HCC progression induced by USP5. Furthermore, administration of WP1130, a USP5 inhibitor, or IMPDH2 reduction by shRNA facilitated the tumor-suppressive role of sorafenib in HCC cells and Huh7 xenograft tumors in nude mice. Together, we identified IMPDH2 as a substrate of USP5, which participates in USP5 induced promotion of HCC progression. Targeting the USP5-IMPDH2 axis might offer potential therapeutic benefits for patients with HCC.
Indexed as
Identifiers
40164869What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.