ArticleNeuromolecular medicine2025
HERC5/ISG15 Enhances Glioblastoma Stemness and Tumor Progression by mediating SERBP1protein stability.
Article in Neuromolecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Article
- Single-Cell Multiomic Profiling Uncovers Radiation Dosage-Sensitive, Cluster-Specific Regulatory Dynamics in Glioblastoma.bioRxiv : the preprint server for biology · 2025Article
- SERBP1: A Multifunctional RNA-Binding Protein Linking Gene Expression, Cellular Metabolism, and Diseases.Cells · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Glioblastoma (GBM) is the most common malignant brain tumor, and has a low survival rate and a poor prognosis. Intensive studies of pathogenic mechanisms are essential for exploring therapeutic targets for GBM. In this study, the roles played by interferon-stimulated gene 15 (ISG15), HECT, RCC1-containing protein 5 (HERC5), and SERPINE1 mRNA binding protein 1 (SERBP1) in regulating GBM cell stemness were investigated. The real-time quantitative polymerase chain reaction (qPCR), western blotting (WB), and immunohistochemistry (IHC) were used to determine the expression levels of HERC5, ISG15, and SERBP1. Cell stemness was analyzed using a cell sphere formation assay. Colony formation and cell counting kit-8 (CCK-8) assays were performed to assess cell proliferation, Transwell assays used to evaluate cell migration and invasion, and flow cytometry was used to assess cell apoptosis after treatment with temozolomide. SERBP1 stability was assessed by a CHX chase assay. A co-immunoprecipitation (Co-IP) assay verified the binding of ISG15 and HERC5 onto SERBP1. Our results showed that HERC5 and ISG15 were highly expressed in GBM. HERC5 and ISG15 promoted the cell stemness of GBM, and increased cell proliferation, sphere formation, migration, invasion, and chemoresistance. Moreover, HERC5 and ISG15 played a synergistic role in promoting the cell stemness of GBM. We also found that HERC5/ISG15 promoted the stability of SERBP1, which also promoted the cell stemness of GBM. The tumor-promoting role of HERC5 and ISG15 was also confirmed in a subcutaneous xenograft tumor model. Collectively, HERC5/ISG15 was found to regulate GBM stemness and tumor progression by mediating SERBP1 protein stability. Our present study suggests a promising therapeutic target for GBM.
Indexed as
Identifiers
39776018What Socratic holds
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 Socratic graph.