ArticleJournal of advanced research2024
The ubiquitin-like protein FAT10 in hepatocellular carcinoma cells limits the efficacy of anti-VEGF therapy.
Article in Journal of advanced research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 2 of them syntheses that pooled it.
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Who cites it
11 citing papers in PubMed, 2 syntheses or guidelines pooled it, 8 citations in OpenAlex.
- Is PD-1/PD-L1 inhibitor plus bevacizumab superior to sorafenib as first-line treatment for advanced hepatocellular carcinoma? A pooled analysis of four phase 3 RCTs.BMC gastroenterology · 2026Pooled it
- Prognostic significance of FAT10 expression in malignant tumors: a systematic review and meta-analysis.Future oncology (London, England) · 2024Pooled it
- Understanding how hypoxia contributes to liver cancer stem cells maintenance.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- The ubiquitin-like protein FAT10 enhances the autophagy-mediated degradation of ZO-1 by stabilizing ATG3 to promote the lung metastasis of colon cancer.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Exploration of the mechanism by which Ubiquitin-like protein UBD promotes malignant progression of breast cancer.Medical oncology (Northwood, London, England) · 2026Article
- Ubiquitin D Correlates with Disease Severity and T Cell Infiltration in Cholestasis: Evidence from Integrated Bioinformatics and Experimental Analyses.International journal of medical sciences · 2026Article
- Pan-cancer multi-omics profiling reveals ubiquitin D as a novel biomarker for diagnosis, immune microenvironment remodeling and prognostic prediction.Discover oncology · 2025Article
- Mechanistic insights into the role of FAT10 in modulating NCOA4-mediated ferroptosis in pancreatic acinar cells during acute pancreatitis.Cell death & disease · 2025Article
- UBE2V1 Promotes Hepatocellular Carcinoma Progression by Forming a Positive Feedback Loop with HIF-1α.Research (Washington, D.C.) · 2025Article
- Article
- FAT10 mediates the sorafenib-resistance of hepatocellular carcinoma cells by stabilizing E3 ligase NEDD4 to enhance PTEN/AKT pathway-induced autophagy.American journal of cancer research · 2024Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionThe efficacy of anti-vascular endothelial growth factor (VEGF) therapy is limited. However, the key factors involved in limiting the efficacy of anti-VEGF therapy and the underlying mechanisms remain unclear.
objectivesTo investigate the effects and mechanisms of human leukocyte antigen F locus-adjacent transcript 10 (FAT10), a ubiquitin-like protein, in limiting the efficacy of anti-VEGF therapy in hepatocellular carcinoma (HCC) cells.
methodsFAT10 was knocked out in HCC cells using the clustered regularly interspaced short palindromic repeats (CRISPR)-CRISPR-associated protein 9 technology. Bevacizumab (BV), an anti-VEGF monoclonal antibody, was used to evaluate the efficacy of anti-VEGF therapy in vivo. Mechanisms of FAT10 action were assessed by RNA sequencing, glutathione S-transferase pulldown assays and in vivo ubiquitination assays.
resultsFAT10 accelerated VEGF-independent angiogenesis in HCC cells which limited BV efficacy and BV-aggravated hypoxia and inflammation promoted FAT10 expression. FAT10 overexpression increased levels of proteins involved in several signaling pathways in HCC cells, resulting in upregulation of VEGF and multiple non-VEGF proangiogenic factors. Upregulation of multiple FAT10-mediated non-VEGF signals compensated for the inhibition of VEGF signaling by BV, enhancing VEGF-independent angiogenesis and promoting HCC growth.
conclusionsOur preclinical findings identify FAT10 in HCC cells as a key factor limiting the efficacy of anti-VEGF therapy and elucidate its underlying mechanisms. This study provides new mechanistic insights into the development of antiangiogenic therapies.
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