BACKGROUND: Glioma recurrence and progression are major causes of poor prognosis and death. Although surgery can provide short-term benefit, long-term outcomes remain limited because effective targets for preventing recurrence and progression are lacking. METHODS: Differentially expressed genes between primary and recurrent gliomas were identified using the CGGA and TCGA databases. The effects of IGFBP2 knockdown on glioma cell proliferation, colony formation, migration, and invasion were assessed by CCK-8, colony formation, migration, and invasion assays. Western blotting was used to investigate the underlying molecular mechanisms. RESULTS: Bioinformatics analysis identified IGFBP2 as a recurrence-associated candidate gene in glioma. High IGFBP2 expression was associated with recurrence status and shorter overall survival. In vitro experiments showed that IGFBP2 knockdown suppressed glioma cell proliferation, colony formation, migration, and invasion. Mechanistically, IGFBP2 knockdown was accompanied by changes in EMT-related markers and reduced AKT/mTOR signaling activity. CONCLUSION: IGFBP2 may serve as a recurrence-associated candidate biomarker and potential therapeutic target in glioma. Further validation using clinical specimens, patient-derived models, orthotopic animal models, and mechanistic rescue experiments is required to confirm its biological and translational significance.
Que et al. (Tue,) studied this question.
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