ArticleCancer research2014
Human Brat ortholog TRIM3 is a tumor suppressor that regulates asymmetric cell division in glioblastoma.
Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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Who cites it
67 citing papers in PubMed, 100 citations in OpenAlex.
- TRIM3 Suppresses Tumor Progression in Non-small-Cell Lung Cancer by Promoting PD-L1 Ubiquitination and Degradation.Annals of surgical oncology · 2026Article
- Orb2 RNA-binding activity promotes neural stem cell development and brain growth in Drosophila larvae.Cell reports · 2026Article
- Review
- Article
- HumaneLife · 2025Article
- A narrative review of papillary thyroid carcinoma-related long non-coding RNAs and their relevance to malignant tumors.Translational cancer research · 2025Review
- Latest News from the "Guardian": p53 Directly Activates Asymmetric Stem Cell Division Regulators.International journal of molecular sciences · 2025Article
- Tripartite-motif 3 represses ovarian cancer progression by downregulating lactate dehydrogenase A and inhibiting AKT signaling.Molecular and cellular biochemistry · 2024Article
- Article
- Advances in the antitumor mechanisms of tripartite motif-containing protein 3.Journal of cancer research and clinical oncology · 2024Review
- TRIM3 inhibits colorectal cancer cell migration and lipid droplet formation by promoting FABP4 degradation.Histology and histopathology · 2024Article
- TRIM3 facilitates ferroptosis in non-small cell lung cancer through promoting SLC7A11/xCT K11-linked ubiquitination and degradation.Cell death and differentiation · 2024Article
- Ribogenesis boosts controlled by HEATR1-MYC interplay promote transition into brain tumour growth.EMBO reports · 2024Article
- Regenerative growth is constrained by brain tumor to ensure proper patterning in Drosophila.PLoS genetics · 2023Article
- Dual roles of TRIM3 in colorectal cancer by retaining p53 in the cytoplasm to decrease its nuclear expression.Cell death discovery · 2023Article
- Overexpression of ST7-AS1 Enhances Apoptosis and Inhibits Proliferation of Papillary Thyroid Carcinoma Cells Via microRNA-181b-5p-Dependent Inhibition Tripartite Motif Containing 3.Molecular biotechnology · 2023Article
- It's a TRIM-endous view from the top: the varied roles of TRIpartite Motif proteins in brain development and disease.Frontiers in molecular neuroscience · 2023Review
- Divergent self-association properties of paralogous proteins TRIM2 and TRIM3 regulate their E3 ligase activity.Nature communications · 2022Article
- TRIM56 promotes malignant progression of glioblastoma by stabilizing cIAP1 protein.Journal of experimental & clinical cancer research : CR · 2022Article
- TRIM3 and TRIM16 as potential tumor suppressors in breast cancer patients.BMC research notes · 2022Article
7 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Cancer stem cells, capable of self-renewal and multipotent differentiation, influence tumor behavior through a complex balance of symmetric and asymmetric cell divisions. Mechanisms regulating the dynamics of stem cells and their progeny in human cancer are poorly understood. In Drosophila, mutation of brain tumor (brat) leads to loss of normal asymmetric cell division by developing neural cells and results in a massively enlarged brain composed of neuroblasts with neoplastic properties. Brat promotes asymmetric cell division and directs neural differentiation at least partially through its suppression on Myc. We identified TRIM3 (11p15.5) as a human ortholog of Drosophila brat and demonstrate its regulation of asymmetric cell division and stem cell properties of glioblastoma (GBM), a highly malignant human brain tumor. TRIM3 gene expression is markedly reduced in human GBM samples, neurosphere cultures, and cell lines and its reconstitution impairs growth properties in vitro and in vivo. TRIM3 expression attenuates stem-like qualities of primary GBM cultures, including neurosphere formation and the expression of stem cell markers CD133, Nestin, and Nanog. In GBM stem cells, TRIM3 expression leads to a greater percentage dividing asymmetrically rather than symmetrically. As with Brat in Drosophila, TRIM3 suppresses c-Myc expression and activity in human glioma cell lines. We also demonstrate a strong regulation of Musashi-Notch signaling by TRIM3 in GBM neurospheres and neural stem cells that may better explain its effect on stem cell dynamics. We conclude that TRIM3 acts as a tumor suppressor in GBM by restoring asymmetric cell division.
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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.