ArticleJournal of extracellular biology2024
ISG15 mediates the function of extracellular vesicles in promoting ovarian cancer progression and metastasis.
Article in Journal of extracellular biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Obesity-driven extracellular vesicle signaling in cancer: mechanistic insights and clinical implications.Oncogenesis · 2026Review
- Organelle-centered ISG15 biology: distinguishing covalent ISGylation from interferon-associated responses.Frontiers in immunology · 2026Review
- Innovations in Oncology Diagnostics: Genetic Research and Liquid Biopsy as Tools of Personalised Medicine.Asian Pacific journal of cancer prevention : APJCP · 2025Review
- The ISGylation tapestry in cancer: weaving phenotypic plasticity through multidimensional regulatory looms.Cellular & molecular biology letters · 2025Review
- ISGylation: is our genome yearning for such a modification?Acta biochimica et biophysica Sinica · 2025Review
- Extracellular vesicles from ovarian cancer tumor spheroids harbor disease-related and survival-associated proteins.Extracellular vesicles and circulating nucleic acids · 2025Article
- Article
- ISG15 mediates the function of extracellular vesicles in promoting ovarian cancer progression and metastasis.Journal of extracellular biology · 2024Article
Corrections and comments
- Erratum issuedCorrection to2025
Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The interferon stimulated gene 15 (ISG15), a ubiquitin like protein and its conjugates have been implicated in various human malignancies. However, its role in ovarian cancer progression and metastasis is largely unknown. In high grade serous ovarian cancer (HGSOC), ascites is the major contributor to peritoneal metastasis. In this study, we identified significantly elevated ISG15 protein expression in HGSOC patient ascites, ascites derived primary ovarian cancer cells (POCCs), POCC small extracellular vesicles (sEVs) as well as metastatic tissue. Our results demonstrates that ISG15 increases exocytosis in ascites-derived POCCs by decreasing the endosome-lysosomal fusion, indicating a key role in sEV secretion. Further, knockdown (KD) of ISG15 resulted in a significant decrease in vesicles secretion from HGSOC cells and
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