ArticleCell death & disease2025
UBE4B promotes gastric cancer proliferation and metastasis by mediating FAT4 ubiquitination and degradation.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- FAT4 loss promotes tumor growth and ferroptosis resistance in hepatocellular carcinoma via PI3K/AKT pathway activation.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- Decreased Expression of FAT4 Promotes Multiple Myeloma Proliferation and Migration by Targeting the Hippo/YAP Pathway.Cancer science · 2026Article
- Research on the role and mechanism of FAT4 in the development and progression of tumor and non-tumor diseases.Discover oncology · 2026Review
- FAT4 restrains epithelial-mesenchymal transition and metastasis in cervical cancer and shapes the tumor immune microenvironment.Journal of translational medicine · 2026Article
- Dual Pathways of UBE4B Inhibit Apoptosis in p53-Positive Tumor Cells via CCAR2 Degradation.International journal of molecular sciences · 2026Article
- Oncogenic SOX9-TRAIP signaling drives gastric cancer progression by mediating the degradation of the CPEB3-mTORC1 tumor suppressor axis.World journal of surgical oncology · 2026Article
- Recent advances in the study of FAT family genes in lung cancer.Discover oncology · 2025Review
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Authors and funding
7 authors.
Funding
Abstract
The ubiquitin‒proteasome system (UPS), an intracellular protein degradation pathway, plays an important role in regulating tumorigenesis and development. Ubiquitination factor E4B (UBE4B/UFD2) has been shown to be associated with the development of several cancers. The aim of this study was to reveal the functional significance of UBE4B in gastric cancer (GC) development and its important mechanism. Bioinformatics analysis, immunohistochemistry (IHC), western blotting, and real-time PCR were performed to detect UBE4B expression in human GC samples and GC cell lines and a mouse xenograft tumour model was established. Our investigation revealed that UBE4B is highly expressed in GC and promotes the proliferation, migration and invasion of GC cells. The quantitative Tandem Mass Tag (TMT) analysis revealed that FAT oncogenic homologue 4 (FAT4) is a downstream gene of UBE4B. Western blot experiments and transmission electron microscopy (TEM) results for biological samples revealed that UBE4B inhibits autophagy in GC cells and directly binds to and degrades FAT4 through ubiquitination. These results suggest that UBE4B can inhibit autophagy and promote GC progression by mediating FAT4 ubiquitination and degradation, and our findings provide a new potential therapeutic target for GC management.
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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.