ArticleOncogenesis2017
MAGE-TRIM28 complex promotes the Warburg effect and hepatocellular carcinoma progression by targeting FBP1 for degradation.
Article in Oncogenesis, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
What it found
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Who cites it
79 citing papers in PubMed, 129 citations in OpenAlex.
- Metabolic Regulation of Immune Responses: Molecular Mechanisms, Diseases, and Therapeutic Targets.MedComm · 2026Review
- TRIM47 Regulates Energy Metabolism via Glycolytic Reprogramming to Drive Hepatocellular Carcinoma Progression and Represents an Efficient Therapeutic Target.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Mitophagy and Ubiquitination Coordinate Context-Specific Mitochondrial Quality Control and EMT/MET Plasticity to Drive Cancer Cell Invasion.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Cross-Species Upregulation ofCurrent issues in molecular biology · 2026Article
- Tripartite motif-containing protein 28 promotes drug resistance to bortezomib in gastric cancer through proteasome activity regulation.CytoJournal · 2026Article
- Targeting the MAGED2-TRIM28-FLNC axis overcomes chemoresistance in TNBC via EMT suppression.Cell communication and signaling : CCS · 2025Article
- Integration of single-cell and bulk transcriptomics to explore prognostic and immunotherapeutic characteristics of sodium overload-induced cell death in lung adenocarcinoma.Translational cancer research · 2025Article
- MLN4924 suppresses tumor metabolism and growth of clear cell renal cell carcinoma by stabilizing nuclear FBP1.Cell death discovery · 2025Article
- O-GlcNAcylation of FBP1 promotes pancreatic cancer progression by facilitating its Lys48-linked polyubiquitination in hypoxic environments.Oncogenesis · 2025Article
- The role of fructose-1,6-bisphosphatase 1 on regulating the cancer progression and drug resistance.Discover oncology · 2025Review
- The impact of metabolic reprogramming in hepatocellular carcinoma on T cell.Frontiers in immunology · 2025Review
- Article
- Multifaceted role ofMedComm · 2024Review
- Calcium-binding protein TgpCaBP regulates calcium storage of the zoonotic parasiteMicrobiology spectrum · 2024Article
- NUP37 accumulation mediated by TRIM28 enhances lipid synthesis to accelerate HCC progression.Oncogene · 2024Article
- Article
- Structural basis for RAD18 regulation by MAGEA4 and its implications for RING ubiquitin ligase binding by MAGE family proteins.The EMBO journal · 2024Article
- DUB3 is a MAGEA3 deubiquitinase and a potential therapeutic target in hepatocellular carcinoma.iScience · 2024Article
- TRIM28 in cancer and cancer therapy.Frontiers in genetics · 2024Review
- TRIM28 facilitates type I interferon activation by targeting TBK1.Frontiers in immunology · 2024Article
19 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
Hepatocellular carcinoma (HCC) is one of the leading cause of cancer death in the world. Fructose-1,6-biphosphatase (FBP1), a rate-limiting enzyme in gluconeogenesis, has been identified recently as a tumor suppressor in HCC and other cancer types. In this study, we demonstrated that the tripartite motif-containing protein 28 (TRIM28) binds directly to and promotes FBP1 for ubiquitination and degradation. MAGE-A3 and MAGE-C2, which are known to be overexpressed in HCC, can enhance TRIM28-dependent degradation of FBP1 by forming ubiquitin ligase complexes with TRIM28. We further showed that expression of TRIM28 increased glucose consumption and lactate production by promoting FBP1 degradation in HCC cells and that FBP1 is a key mediator of TRIM28-induced HCC growth in culture and in mice. Moreover, we demonstrated that FBP1 and TRIM28 protein levels inversely correlated in HCC patient specimens. Finally, we showed that the proteasome inhibitor bortezomib mitigated the Warburg effect by inhibiting FBP1 degradation in HCC. Collectively, our findings not only identify oncogenic MAGE-TRIM28 complex-mediated proteasome degradation of FBP1 as a key mechanism underlying downregulation of FBP1 proteins in HCC, but also reveal that MAGE-TRIM28-regulated reprogramming of cancer cell metabolism and HCC tumorigenesis is mediated, at least in part, through FBP1 degradation.
Identifiers
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.