ArticleCell communication and signaling : CCS2026
USP5 inhibition stimulates immunogenic ferroptosis that enhances immunotherapy in diffuse large B-cell lymphoma.
Article in Cell communication and signaling : CCS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- USP5 in cancer: a therapeutic window into metabolism and drug resistance.Journal of translational medicine · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
backgroundAdvances in immunotherapy have transformed the treatment landscape for diffuse large B-cell lymphoma (DLBCL), but drug resistance continues to limit its clinical efficacy. Ferroptosis, a form of immunogenic cell death, is critical for promoting adaptive anti-tumor immunity. Here, we report the role of Ubiquitin specific peptidase 5 (USP5) in regulating ferroptosis and immune evasion in DLBCL.
methodsThe study employed in vitro and in vivo models of DLBCL to investigate the role of USP5 in ferroptosis and immune evasion. The main techniques included cell proliferation analysis, single-cell RNA sequencing, immunofluorescence, western blotting, microplate reader assays, and mouse xenograft models. The interaction between USP5 and insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3) was confirmed through mass spectrometry, co-immunoprecipitation, and surface plasmon resonance, with further functional assessment conducted using rescue experiments.
resultsUSP5 is highly expressed in DLBCL, and its deletion suppresses tumor growth in an immune system-dependent manner by enhancing the infiltration and activation of CD8+ T cells. Mechanistically, USP5 directly interacts with, deubiquitinates, and stabilizes IGF2BP3, thereby maintaining the mRNA stability of anti-ferroptotic factors and preventing ferroptosis and the release of damage-associated molecular patterns (DAMPs). Furthermore, USP5 inhibition significantly enhances the efficacy of anti-PD1 therapy via ferroptosis-mediated anti-tumor immunity in DLBCL mouse xenograft models.
conclusionsCollectively, our study reveals a critical role for the USP5-IGF2BP3 axis in suppressing immunogenic ferroptosis and provides a promising therapeutic target for DLBCL immunotherapy.
Indexed as
Identifiers
What 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.