ReviewJournal of translational medicine2026
Mechanisms and functions of the TRIM protein family in digestive system cancers.
Review in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
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Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTripartite motif-containing (TRIM) proteins are important RING-type E3 ubiquitin ligases that regulate protein fate and signal transduction through ubiquitin/ubiquitin-like modifications and non-ubiquitination mechanisms. In digestive system cancers, TRIM proteins exert highly context-dependent bidirectional effects. Here, we conceptualize TRIM proteins as signal integration nodes linking ubiquitin-mediated regulation, core signaling pathways, and adaptation to the tumor microenvironment.
methodsThis structured narrative review synthesizes English-language studies indexed in PubMed between January 2010 and October 2025. It focuses on the structural basis, multilevel regulation, molecular networks, phenotypic functions, prognostic relevance, and therapeutic implications of TRIM proteins in esophageal squamous cell carcinoma, gastric cancer, colorectal cancer, hepatocellular carcinoma, and pancreatic ductal adenocarcinoma.
conclusionsThe modular architecture of TRIM proteins enables diverse substrate recognition and regulatory outputs. Cross-cancer analysis identifies pathway-convergent, phenotype-convergent, and pathway-phenotype bridging TRIM members that translate dysregulation of core pathways, including Wnt/β-catenin, PI3K/AKT, and p53, into proliferative, cell death-related, metastatic, metabolic, and immune phenotypes. Their functional direction is jointly shaped by tumor type, molecular subtype, substrate status, microenvironmental cues, and treatment context. Selected TRIM members show potential as prognostic biomarkers, risk-stratification indicators, and predictors of therapeutic response, whereas most TRIM-targeted strategies remain preclinical. Future studies should clarify ubiquitin-chain-specific regulatory logic, subtype-specific functions, and multilayered networks, while rigorously evaluating the specificity, safety, and clinical applicability of TRIM-directed combination therapies.
Indexed as
Identifiers
42919382What 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.