ArticleNature communications2017
TRIM24 is an oncogenic transcriptional co-activator of STAT3 in glioblastoma.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.
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
92 citing papers in PubMed, 166 citations in OpenAlex.
- TRIM24 in Human Cancers: A Dual-Function Oncoprotein, Regulatory Mechanisms, and Emerging Therapeutic Strategies.International journal of cancer · 2026Review
- Epigenetic programming by H3K23ac defines lineage fate of Meg3Nature cell biology · 2026Article
- Article
- Nicotinamide prevents anti-PD1 immune checkpoint inhibitor-associated early stages of cardiotoxicity.Science China. Life sciences · 2026Article
- Prognostic value of TRIM24 expression in gastric cancer and various human solid tumours: a comprehensive cross-sectional, and meta-analysis study.Przeglad gastroenterologiczny · 2026Article
- Comprehensive characterization and targeted treatment of a pediatric epithelioid glioblastoma with a rare TRIM24-NTRK2 fusion.NPJ precision oncology · 2025Article
- A structurally informed human protein-protein interactome reveals proteome-wide perturbations caused by disease mutations.Nature biotechnology · 2025Article
- Systematic analysis identifies TRIM22 as an oncogenic and immunological biomarker in glioma.BMC cancer · 2025Article
- TRIM24 regulates chromatin remodeling and calcium dynamics in cardiomyocytes.Cell communication and signaling : CCS · 2025Article
- Comprehensive exome profiling identifiesTheranostics · 2025Article
- Mechanism of Curcumin in Inhibiting Proliferation of Head and Neck Squamous Cell Carcinoma: A Network Pharmacology and Cellular Experimental Study.BioMed research international · 2025Article
- Lipid Nanoparticles as a Platform for miRNA and siRNA Delivery in Hepatocellular Carcinoma.Current drug delivery · 2025Review
- Potential of Natural Products in the Treatment of Glioma: Focus on Molecular Mechanisms.Cell biochemistry and biophysics · 2024Review
- The tripartite motif-containing 24 is a multifunctional player in human cancer.Cell & bioscience · 2024Review
- TRIM24 Cooperates with Ras Mutation to Drive Glioma Progression through snoRNA Recruitment of PHAX and DNA-PKcs.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The deubiquitinase USP7 and E3 ligase TRIM21 regulate vasculogenic mimicry and malignant progression of RMS by balancing SNAI2 homeostasis.Journal of experimental & clinical cancer research : CR · 2024Article
- Structurally-informed human interactome reveals proteome-wide perturbations by disease mutations.bioRxiv : the preprint server for biology · 2024Article
- USP7 inhibits the progression of nasopharyngeal carcinoma via promoting SPLUNC1-mediated M1 macrophage polarization through TRIM24.Cell death & disease · 2023Article
- EGFR promotes ALKBH5 nuclear retention to attenuate N6-methyladenosine and protect against ferroptosis in glioblastoma.Molecular cell · 2023Article
- Targeting TRIM24 promotes neuroblastoma differentiation and decreases tumorigenicity via LSD1/CoREST complex.Cellular oncology (Dordrecht, Netherlands) · 2023Article
32 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Aberrant amplification and mutations of epidermal growth factor receptor (EGFR) are the most common oncogenic events in glioblastoma (GBM), but the mechanisms by which they promote aggressive pathogenesis are not well understood. Here, we determine that non-canonical histone signature acetylated H3 lysine 23 (H3K23ac)-binding protein tripartite motif-containing 24 (TRIM24) is upregulated in clinical GBM specimens and required for EGFR-driven tumorigenesis. In multiple glioma cell lines and patient-derived glioma stem cells (GSCs), EGFR signaling promotes H3K23 acetylation and association with TRIM24. Consequently, TRIM24 functions as a transcriptional co-activator and recruits STAT3, leading to stabilized STAT3-chromatin interactions and subsequent activation of STAT3 downstream signaling, thereby enhancing EGFR-driven tumorigenesis. Our findings uncover a pathway in which TRIM24 functions as a signal relay for oncogenic EGFR signaling and suggest TRIM24 as a potential therapeutic target for GBM that are associated with EGFR activation.
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.