ArticleNPJ precision oncology2025
MYSM1 promotes lung adenocarcinoma progression via TRAF2/3-mediated activation of MAPK and non-canonical NF-κB pathways.
Article in NPJ precision oncology, 2025. 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
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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.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
9 authors.
Funding
Abstract
MYSM1, a deubiquitinating enzyme, is markedly overexpressed in lung adenocarcinoma (LUAD) and correlates with advanced disease stage and poor prognosis. Functional assays demonstrated that MYSM1 promotes LUAD cell proliferation and migration in vitro and in vivo. Mechanistically, MYSM1 interacts with TRAF2 and TRAF3 via its SWIRM domain, removing K63-linked polyubiquitin chains to decrease TRAF2-TRAF3 complex stability. This process impairs NIK degradation and sustains non-canonical NF-κB activation while simultaneously promoting MAPK (p38, JNK) signal pathway. Rescue experiments indicate that inhibiting TRAF2 or TRAF3 can attenuate MYSM1-induced activation of the MAPK pathway. These findings identify MYSM1 as a novel regulator of TRAF2-TRAF3 complex stability and a potential prognostic biomarker and therapeutic target in LUAD.
Identifiers
What Socratic holds
Registered trials
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