ArticleCell communication and signaling : CCS2023
The deubiquitinase EIF3H promotes hepatocellular carcinoma progression by stabilizing OGT and inhibiting ferroptosis.
Article in Cell communication and signaling : CCS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Emerging roles of O-GlcNAcylation in tumorigenesis, immunosuppression and drug resistance (Review).Oncology letters · 2026Review
- EIF3H Modulates Glycolysis Through LDHA Stabilization in Triple-Negative Breast Cancer.Cancers · 2026Article
- Deubiquitinating Enzymes as Therapeutic Candidates in Hepatocellular Carcinoma and Other Liver Disease.International journal of molecular sciences · 2026Review
- Deubiquitinases in liver diseases: from mechanisms to targeted therapy.Science China. Life sciences · 2026Review
- EIF3B regulates the cell cycle of lung adenocarcinoma cells by activating the GTSE1 mediated ERK/MAPK pathway.Respiratory research · 2026Article
- RPLP0 identified as a ferroptosis regulator in HCC through pan-cancer analysis.Frontiers in oncology · 2026Article
- Tks5 interactome reveals endoplasmic-reticulum-associated translation machinery in invadosomes.The FEBS journal · 2025Article
- Mechanisms of ferroptosis in primary hepatocellular carcinoma and progress of artificial intelligence-based predictive modeling in hepatocellular carcinoma.World journal of gastroenterology · 2025Review
- ULK1-dependent phosphorylation of OGT instructs the tumorigenicity of O-GlcNAcylation.Science China. Life sciences · 2025Article
- O‑GlcNAcylation as an emerging molecular target for cholangiocarcinoma therapy (Review).Oncology reports · 2025Review
- A ROS-mediated oxidation-O-GlcNAcylation cascade governs ferroptosis.Nature cell biology · 2025Article
- Targeting RPLP2 Triggers DLBCL Ferroptosis by Decreasing FXN Expression.Biomedicines · 2025Article
- Pharmacological Dissection Identifies Retatrutide Overcomes the Therapeutic Barrier of Obese TNBC Treatments through Suppressing the Interplay between Glycosylation and Ubiquitylation of YAP.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Cancer-associated fibroblasts promote doxorubicin resistance in triple-negative breast cancer through enhancing ZFP64 histone lactylation to regulate ferroptosis.Journal of translational medicine · 2025Article
- FBXO31-mediated ubiquitination of OGT maintains O-GlcNAcylation homeostasis to restrain endometrial malignancy.Nature communications · 2025Article
- Review
- Deubiquitinating enzymes: Key regulators of ferroptosis and pyroptosis and novel targets for cancer intervention.International journal of biological sciences · 2025Review
- CARM1-mediated OGT arginine methylation promotes non-small cell lung cancer glycolysis by stabilizing OGT.Cell death & disease · 2024Article
- KDM2B regulates stroke injury by modulating OGT-mediated 0-GlcNAcylation of SLC7A11.Communications biology · 2024Article
- Unlocking hepatocellular carcinoma aggression: STAMBPL1-mediated TRAF2 deubiquitination activates WNT/PI3K/NF-kb signaling pathway.Biology direct · 2024Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) is one of the most prevalent and lethal human malignancies, and with quite limited treatment alternatives. The proteasome is responsible for most of the protein degradation in eukaryotic cells and required for the maintenance of intracellular homeostasis. However, its potential role in HCC is largely unknown. In the current study, we identified eukaryotic translation initiation factor 3 subunit H (EIF3H), belonging to the JAB1/MPN/MOV34 (JAMM) superfamily, as a bona fide deubiquitylase of O-GlcNAc transferase (OGT) in HCC. We explored that EIF3H was positively associated with OGT in HCC and was related to the unfavorable prognosis. EIF3H could interact with, deubiquitylate, and stabilize OGT in a deubiquitylase-dependent manner. Specifically, EIF3H was associated with the GT domain of ERα via its JAB/MP domain, thus inhibiting the K48-linked ubiquitin chain on OGT. Besides, we demonstrated that the knockdown of EIF3H significantly reduced OGT protein expression, cell proliferation and invasion, and caused G1/S arrest of HCC. We also found that the deletion of EIF3H prompted ferroptosis in HCC cells. Finally, the effects of EIF3H depletion could be reversed by further OGT overexpression, implying that the OGT status is indispensable for EIF3H function in HCC carcinogenesis. In summary, our study described the oncogenic function of EIF3H and revealed an interesting post-translational mechanism between EIF3H, OGT, and ferroptosis in HCC. Targeting the EIF3H may be a promising approach in HCC. Video Abstract.
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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 Socratic graph.