ArticleJournal of experimental & clinical cancer research : CR2022
TRIM56 promotes malignant progression of glioblastoma by stabilizing cIAP1 protein.
Article in Journal of experimental & clinical cancer research : CR, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- Pooled it
- mCell death & disease · 2026Article
- PHF23-Related Prognostic Signature Modulates Immune Microenvironment and Promotes Tumor Malignancy in Glioma.International journal of molecular sciences · 2026Article
- Induction of TRIM22 promotes autophagy and apoptosis of colorectal cancer through reactive oxygen species generation.Journal of translational medicine · 2026Article
- TRIM47-facilitated PLK1 stabilization promotes the proliferation of liver cancer cells.Cellular oncology (Dordrecht, Netherlands) · 2025Article
- E3 ubiquitin ligase BTRC inhibits the proliferation and tumor growth of glioma cells through the NFAT5/AQP4 axis.Journal of cancer research and clinical oncology · 2025Article
- TRIM56 enhances adenoviral E1A steady state to improve oncolytic adenovirus therapy efficacy.Journal of virology · 2025Article
- E3 ligase TRIM22 promotes melanoma proliferation by regulating cell cycle progression through K63-linked ubiquitination of p21.Scientific reports · 2025Article
- The oncogenic role of TRIM56 in pancreatic cancer via the TRAF6/NF-kB axis.Journal of molecular histology · 2025Article
- Comprehensive analysis of TRIM56's prognostic value and immune infiltration in Pan-Cancer.Scientific reports · 2025Article
- TRIM56 Promotes White Adipose Tissue Browning to Attenuate Obesity by Degrading TLE3.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The regulation of innate antiviral immunity by TRIM56.Infectious diseases & immunity · 2025Review
- Super-enhancer-driven SLCO4A1-AS1 is a new biomarker and a promising therapeutic target in glioblastoma.Scientific reports · 2025Article
- Beyond Tumors: The Pivotal Role of TRIM Proteins in Chronic Non-Tumor Lung Diseases.Journal of inflammation research · 2025Review
- Neutrophil extracellular traps aggravate neuronal apoptosis and neuroinflammation via neddylation after traumatic brain injury.Theranostics · 2025Article
- NAP1L1 regulates BIRC2 ubiquitination modification via E3 ubiquitin ligase UBR4 and hence determines hepatocellular carcinoma progression.Cell death discovery · 2024Article
- Article
- Stabilization of KPNB1 by deubiquitinase USP7 promotes glioblastoma progression through the YBX1-NLGN3 axis.Journal of experimental & clinical cancer research : CR · 2024Article
- ZNF503-AS2 is a promising therapeutic target and is associated with the immune microenvironment in glioma.PloS one · 2024Article
- Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe tripartite motif (TRIM) family of proteins plays a key role in the developmental growth and therapeutic resistance of many tumors. However, the regulatory mechanisms and biological functions of TRIM proteins in human glioblastoma (GBM) are not yet fully understood. In this study, we focused on TRIM56, which emerged as the most differentially expressed TRIM family member with increased expression in GBM.
methodsWestern blot, real-time quantitative PCR (qRT-PCR), immunofluorescence (IF) and immunohistochemistry (IHC) were used to study the expression levels of TRIM56 and cIAP1 in GBM cell lines. Co-immunoprecipitation (co-IP) was used to explore the specific binding between target proteins and TRIM56. A xenograft animal model was used to verify the tumor promoting effect of TRIM56 on glioma in vivo.
resultsWe observed elevated expression of TRIM56 in malignant gliomas and revealed that TRIM56 promoted glioma progression in vitro and in a GBM xenograft model in nude mice. Analysis of the Human Ubiquitin Array and co-IPs showed that cIAP1 is a protein downstream of TRIM56. TRIM56 deubiquitinated cIAP1, mainly through the zinc finger domain (amino acids 21-205) of TRIM56, thereby reducing the degradation of cIAP1 and thus increasing its expression. TRIM56 also showed prognostic significance in overall survival of glioma patients.
conclusionsTRIM56-regulated post-translational modifications may contribute to glioma development through stabilization of cIAP1. Furthermore, TRIM56 may serve as a novel prognostic indicator and therapeutic molecular target for GBM.
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