ArticleJournal of Cancer2024
High Expression of RAB32 Predicts Adverse Outcomes: A Potential Therapeutic Target for Glioblastoma.
Article in Journal of Cancer, 2024. 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
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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.
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.
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Who cites it
3 citing papers in PubMed.
- Clinical Significance of RBM15 in Gastric Cancer: A Multi-Database Validation.Current medicinal chemistry · 2026Article
- Characterization of T cell markers in endometrial carcinoma through single-cell RNA sequencing.Discover oncology · 2025Article
- Rab32 regulates Golgi structure and cell migration through Protein Kinase A-mediated phosphorylation of Optineurin.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
RAB32 is a potential prognostic marker that is overexpressed in a variety of cancers. The purpose of this study was to investigate the expression and function of RAB32 in glioblastoma (GBM). The RAB32 expression data were obtained by accessing the TCGA, CGGA and GEPIA databases and were verified by western blot and immunohistochemistry. The prognostic value of RAB32 methylation was carefully examined using cBioPortal and MethSurv. GSEA was used to analyze cancer-related signaling pathways that may be activated by high RAB32 expression. The correlation between RAB32 and GBM infiltration was studied by accessing the TISIDB database. The effects of RAB32 on the proliferation, migration and invasion of GBM cells were predicted by colony formation assay, CCK-8 assay and Transwell assay. In this study, RAB32 expression was upregulated in GBM compared to normal brain tissue. Survival analysis showed that high expression of RAB32 was an independent risk factor for overall survival in glioma patients. RAB32 methylation was negatively correlated with RAB32 expression, and the overall survival rate of patients with RAB32 hypomethylation was lower than that of patients with RAB32 hypermethylation. Through functional enrichment analysis, we found that RAB32 overexpression significantly activated multiple signaling pathways. The immunoassay results showed that RAB32 expression was correlated with immune infiltration of the tumor microenvironment. Knocking down the expression of the RAB32 gene significantly inhibited the proliferation, migration and invasion of glioma cells. Our results show that RAB32 is a key factor affecting the prognosis of patients with GBM, and its targeting may provide a new treatment for patients with GBM.
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