ArticleFrontiers in cell and developmental biology2022
The Dual Roles of MAGE-C2 in p53 Ubiquitination and Cell Proliferation Through E3 Ligases MDM2 and TRIM28.
Article in Frontiers in cell and developmental biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 15 citations in OpenAlex.
- MAGEC2 promotes tumorigenesis in multiple myeloma through USP16-mediated deubiquitination and stabilization of c-Myc.Experimental hematology & oncology · 2026Article
- Insights into X-Linked Susceptibility to Parkinson's Disease in the South African Population.medRxiv : the preprint server for health sciences · 2025Article
- ALDH4A1 knockdown inhibits in vitro atherosclerosis model by modulating Trim28-mediated P53 ubiquitination to suppress ferroptosis of vascular endothelial cells.In vitro cellular & developmental biology. Animal · 2025Article
- Development of Next Generation Cell-Permeable Peptide Inhibitors for the Oncological Target MAGE-A4.Journal of medicinal chemistry · 2025Article
- A novel indirubin- 3-monoxime derivative I3MV- 8b exhibits remarkable cytotoxicity against multiple myeloma by targeting TRIM28.Biomarker research · 2025Article
- KAP1 in antiviral immunity: dual roles in viral silencing and immune regulation.Frontiers in cellular and infection microbiology · 2025Review
- PPIXpress and PPICompare webservers infer condition-specific and differential PPI networks.Bioinformatics advances · 2025Article
- Cancer testis antigens: Emerging therapeutic targets leveraging genomic instability in cancer.Molecular therapy. Oncology · 2024Review
- TRIM28 in cancer and cancer therapy.Frontiers in genetics · 2024Review
- The SUMOylation and ubiquitination crosstalk in cancer.Journal of cancer research and clinical oncology · 2023Review
- Article
- MiRNA Differences Related to Treatment-Resistant Schizophrenia.International journal of molecular sciences · 2023Article
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6 authors at 1 institution in 1 country.
Funding
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Abstract
The tumor suppressor p53 is critical for the maintenance of genome stability and protection against tumor malignant transformation, and its homeostasis is usually regulated by ubiquitination. MDM2 is a major E3 ligase of p53 ubiquitination, and its activity is enhanced by TRIM28. TRIM28 also independently ubiquitinates p53 as an E3 ligase activated by MAGE-C2. Moreover, MAGE-C2 is highly expressed in various cancers, but the detailed mechanisms of MAGE-C2 involved in MDM2/TRIM28-mediated p53 ubiquitination remain unknown. Here, we found that MAGE-C2 directly interacts with MDM2 through its conserved MHD domain to inhibit the activity of MDM2 on p53 ubiquitination. Furthermore, TRIM28 acts as an MAGE-C2 binding partner and directly competes with MAGE-C2 for MDM2 interaction, thus releasing the inhibitory role of MAGE-C2 and promoting p53 ubiquitination. MAGE-C2 suppresses cell proliferation in TRIM28-deficient cells, but the overexpression of TRIM28 antagonizes the inhibitory role of MAGE-C2 and accumulates p53 ubiquitination to promote cell proliferation. This study clarified the molecular link of MAGE-C2 in two major E3 systems MDM2 and TRIM28 on p53 ubiquitination. Our results revealed the molecular function of how MAGE-C2 and TRIM28 contribute to p53 ubiquitination and cell proliferation, in which MAGE-C2 acts as a potential inhibitor of MDM2 and TRIM28 is a vital regulator for MAGE-C2 function in p53 protein level and cell proliferation. This work would be helpful to understand the regulation mechanism of tumor suppressor p53.
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