ArticleCancer research2018
TRIM59 Promotes Gliomagenesis by Inhibiting TC45 Dephosphorylation of STAT3.
Article in Cancer research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 34 papers, 2 of them syntheses that pooled it.
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.
Who cites it
34 citing papers in PubMed, 2 syntheses or guidelines pooled it, 60 citations in OpenAlex.
- Tracing the origins of glioblastoma by investigating the role of gliogenic and related neurogenic genes/signaling pathways in GBM development: a systematic review.World journal of surgical oncology · 2022Pooled it
- Prognostic significance of TRIM59 for cancer patient survival: A systematic review and meta-analysis.Medicine · 2019Pooled it
- TRIM59 promotes immune evasion and tumor progression in lung adenocarcinoma via ubiquitin- proteasomal degradation of IRF3.Frontiers in immunology · 2026Article
- Targeting TRIM59 impairs RNA splicing and promotes neuroblastoma differentiation and therapeutic responses.Journal of experimental & clinical cancer research : CR · 2025Article
- Multifaceted role ofMedComm · 2024Review
- TRIM25, TRIM28 and TRIM59 and Their Protein Partners in Cancer Signaling Crosstalk: Potential Novel Therapeutic Targets for Cancer.Current issues in molecular biology · 2024Review
- ETHE1 dampens colorectal cancer angiogenesis by promoting TC45 Dephosphorylation of STAT3 to inhibit VEGF-A expression.Cell death & disease · 2024Article
- CDK2-activated TRIM32 phosphorylation and nuclear translocation promotes radioresistance in triple-negative breast cancer.Journal of advanced research · 2024Article
- KAP1 stabilizes MYCN mRNA and promotes neuroblastoma tumorigenicity by protecting the RNA mJournal of experimental & clinical cancer research : CR · 2024Article
- Review
- Extracellular vesicle-derived CircWhsc1 promotes cardiomyocyte proliferation and heart repair by activating TRIM59/STAT3/Cyclin B2 pathway.Journal of advanced research · 2023Article
- LPS inhibits TRIM65 expression in macrophages and C57BL/6J mouse by activating the ERK1/2 signaling pathway.Experimental and therapeutic medicine · 2023Article
- SARS-CoV-2 viral protein ORF3A injures renal tubules by interacting with TRIM59 to induce STAT3 activation.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- A bio-orthogonal linear ubiquitin probe identifies STAT3 as a direct substrate of OTULIN in glioblastoma.Nucleic acids research · 2023Article
- Article
- TRIM8: a double-edged sword in glioblastoma with the power to heal or hurt.Cellular & molecular biology letters · 2023Review
- Nuclear receptor coactivator SRC-1 promotes colorectal cancer progression through enhancing GLI2-mediated Hedgehog signaling.Oncogene · 2022Article
- TRIM32 promotes radioresistance by disrupting TC45-STAT3 interaction in triple-negative breast cancer.Oncogene · 2022Article
- Identification of a tripartite motif family gene signature for predicting the prognosis of patients with glioma.American journal of translational research · 2022Article
- TRIM59 promotes osteosarcoma progression via activation of STAT3.Human cell · 2022Article
Corrections and comments
- Expression of concern
Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
Aberrant EGFR signaling is a common driver of glioblastoma (GBM) pathogenesis; however, the downstream effectors that sustain this oncogenic pathway remain unclarified. Here we demonstrate that tripartite motif-containing protein 59 (TRIM59) acts as a new downstream effector of EGFR signaling by regulating STAT3 activation in GBM. EGFR signaling led to TRIM59 upregulation through SOX9 and enhanced the interaction between TRIM59 and nuclear STAT3, which prevents STAT3 dephosphorylation by the nuclear form of T-cell protein tyrosine phosphatase (TC45), thereby maintaining transcriptional activation and promoting tumorigenesis. Silencing TRIM59 suppresses cell proliferation, migration, and orthotopic xenograft brain tumor formation of GBM cells and glioma stem cells. Evaluation of GBM patient samples revealed an association between EGFR activation, TRIM59 expression, STAT3 phosphorylation, and poor prognoses. Our study identifies TRIM59 as a new regulator of oncogenic EGFR/STAT3 signaling and as a potential therapeutic target for GBM patients with EGFR activation.
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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.