ReviewInternational journal of cancer2026
TRIM24 in Human Cancers: A Dual-Function Oncoprotein, Regulatory Mechanisms, and Emerging Therapeutic Strategies.
Review in International journal of cancer, 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
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0 citing papers in PubMed.
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Authors and funding
10 authors.
Funding
Abstract
The tripartite motif-containing protein 24 (TRIM24) functions as a pivotal epigenetic scaffold and E3 ubiquitin ligase, orchestrating tumorigenesis through context-dependent dual roles. While frequently amplified in cancers such as prostate and breast carcinoma-where it drives oncogenesis via Wnt/β-catenin and PI3K/AKT pathway activation-emerging evidence positions TRIM24 as a tumor suppressor in specific contexts, modulating retinoic acid signaling and macrophage polarization. This dichotomy is governed by intricate post-translational modifications (PTMs), including phosphorylation-dependent nucleocytoplasmic shuttling and SUMOylation, which dictate substrate specificity for targets ranging from p53 to VHL. Furthermore, TRIM24 operates within a complex non-coding RNA network (e.g., miRNA-511, lncRNA NCK1-AS1) that fine-tunes its oncogenic output. Clinically, aberrant TRIM24 expression correlates with poor prognosis and therapeutic resistance across multiple malignancies. Mechanistically, its unique PHD-Bromo dual-domain structure confers specific recognition of the noncanonical H3K4me0/H3K23ac histone signature, presenting a compelling therapeutic target. Current strategies, including PROTAC degraders and allosteric inhibitors targeting its bromodomain or downstream effectors (e.g., DNA-PKcs, AURKB), demonstrate significant preclinical efficacy. This review synthesizes the molecular circuitry of TRIM24, elucidates the determinants of its functional switch, and evaluates emerging precision medicine approaches to overcome resistance in TRIM24-addicted tumors.
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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.