ArticleExperimental & molecular medicine2023
TRIM22 promotes the proliferation of glioblastoma cells by activating MAPK signaling and accelerating the degradation of Raf-1.
Article in Experimental & molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 37 citations in OpenAlex.
- Lcn2 Promotes Ferroptosis in Intracerebral Hemorrhage by Targeting Keap1 Tyr572 and Restricting Nrf2 Activation.MedComm · 2026Article
- Myrtenol modulates TWEAK/TLR4-NF-κB, miR-21, PTEN, and ERK-1 expressions and improves behavioral outcomes in a rat glioblastoma model.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Induction of TRIM22 during Clonorchis sinensis infection triggers intracellular ROS accumulation by suppressing the mTOR-mediated Nrf2 signaling pathway.Genes & genomics · 2026Article
- Identifying Key Pathogenic Mechanisms in Recurrent Glioblastoma Through Bioinformatics Analysis.Current medicinal chemistry · 2026Article
- SPP1+ macrophages polarized by lactate confer the progression of hypoxic adaptive tumor cells in brain.Neuro-oncology · 2026Article
- Systematic analysis identifies TRIM22 as an oncogenic and immunological biomarker in glioma.BMC cancer · 2025Article
- E3 ligase TRIM22 promotes melanoma proliferation by regulating cell cycle progression through K63-linked ubiquitination of p21.Scientific reports · 2025Article
- Article
- Single-Nucleus RNA Sequencing Reveals That Gabra6Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- TRIM22 functions as a scaffold protein for autophagy initiation.Animal cells and systems · 2025Article
- Microglial Lcn2 knockout enhances chronic intracerebral hemorrhage recovery by restoring myelin and reducing inflammation.Theranostics · 2025Article
- TRIM22 promotes glioblastoma development by ubiquitinating Bcl-2.Molecular & cellular oncology · 2025Article
- Integrating cuproptosis- and ferroptosis-related gene signatures to predict prognosis, immunotherapy response, and drug sensitivity in patients with skin cutaneous melanoma.Frontiers in immunology · 2025Article
- Multifaceted role ofMedComm · 2024Review
- Emerging roles of tripartite motif family proteins (TRIMs) in breast cancer.Cancer medicine · 2024Review
- Activation of AMPK inhibits cervical cancer growth by hyperacetylation of H3K9 through PCAF.Cell communication and signaling : CCS · 2024Article
- SP140 inhibitor suppressing TRIM22 expression regulates glioma progress through PI3K/AKT signaling pathway.Brain and behavior · 2024Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tripartite motif (TRIM) 22 and mitogen-activated protein kinase (MAPK) signaling pathways play critical roles in the growth of glioblastoma (GBM). However, the molecular mechanism underlying the relationship between TRIM22 and MAPK signaling remains unclear. Here, we found that TRIM22 binds to exon 2 of the sphingosine kinase 2 (SPHK2) gene. An ERK1/2-driven luciferase reporter construct identified TRIM22 as a potential activator of MAPK signaling. Knockout and overexpression of TRIM22 regulate the inhibition and activation of MAPK signaling through the RING-finger domain. TRIM22 binds to Raf-1, a negative regulator of MAPK signaling, and accelerates its degradation by inducing K48-linked ubiquitination, which is related to the CC and SPRY domains of TRIM22 and the C1D domain of Raf-1. In vitro and in vivo, an SPHK2 inhibitor (K145), an ERK1/2 inhibitor (selumetinib), and the nonphosphorylated mutant Raf-1
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