ArticleOncogene2022
Extracellular vesicles-transferred SBSN drives glioma aggressiveness by activating NF-κB via ANXA1-dependent ubiquitination of NEMO.
Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Article
- Periodontitis-Associated Circulating EVs Promote Colorectal Cancer Progression via Carnosine-Mediated Acidosis Adaptation.Cell proliferation · 2026Article
- An LCN2-Dependent Positive-Feedback Loop Between Gastric Cancer Cells and Tumor-Associated-Macrophages Mediates Lymphangiogenesis and Lymphatic Metastasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Suprabasin promotes gastric cancer liver metastasis via hepatic stellate cells-mediated EGF/CCL2/JAK2 intercellular signaling pathways.Oncogene · 2025Article
- The new advance of exosome-based liquid biopsy for cancer diagnosis.Journal of nanobiotechnology · 2024Review
- TRIM Expression in HNSCC: Exploring the Link Between Ubiquitination, Immune Infiltration, and Signaling Pathways Through Bioinformatics.International journal of general medicine · 2024Article
- The role of extracellular vesicles in circulating tumor cell-mediated distant metastasis.Molecular cancer · 2023Review
Corrections and comments
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Authors and funding
22 authors at 8 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioma is the most common malignant primary brain tumor with aggressiveness and poor prognosis. Although extracellular vesicles (EVs)-based cell-to-cell communication mediates glioma progression, the key molecular mediators of this process are still not fully understood. Herein, we elucidated an EVs-mediated transfer of suprabasin (SBSN), leading to the aggressiveness and progression of glioma. High levels of SBSN were positively correlated with clinical grade, predicting poor clinical prognosis of patients. Upregulation of SBSN promoted, while silencing of SBSN suppressed tumorigenesis and aggressiveness of glioma cells in vivo. EVs-mediated transfer of SBSN resulted in an increase in SBSN levels, which promoted the aggressiveness of glioma cells by enhancing migration, invasion, and angiogenesis of recipient glioma cells. Mechanistically, SBSN activated NF-κB signaling by interacting with annexin A1, which further induced Lys63-linked and Met1-linear polyubiquitination of NF-κB essential modulator (NEMO). In conclusion, the communication of SBSN-containing EVs within glioma cells drives the formation and development of tumors by activating NF-κB pathway, which may provide potential therapeutic target for clinical intervention in glioma.
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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.