<p>SKP2 (S-phase kinase-associated protein 2) plays an important role in the regulation of the cell cycle, tumorigenesis, progression, and metastasis. However, its functional role in gliomas is currently unclear. This study aimed to investigate the relationship between SKP2 and the progression of gliomas, and its effects on the glioma cell cycle. The relationship between SKP2 expression levels and clinical characteristics of gliomas was explored in our datasets. Kaplan–Meier analysis and COX regression were conducted to evaluate the prognostic role of SKP2. Differentially expressed genes were identified between high and low SKP2 groups. The function and related mechanisms of SKP2 were evaluated based on Gene Ontology and Gene Set Enrichment Analysis. LASSO-Cox was used to screen the variables, and the prediction model was established by nomogram analysis. The effects of SKP2 on the glioma cell cycle were examined in cellular experiments. The SKP2 expression level was positively correlated with adverse clinical features of gliomas, and overall survival with high SKP2 expression was significantly shortened. Gene enrichment analysis showed that the differential genes in the SKP2 high-expression group were mainly enriched in cell cycle and mitosis. In vitro experiments confirmed that silencing of SKP2 arrested the glioma cell cycle at the G1 phase in both U87 and U251 cells. In conclusion, SKP2 may serve as a potential prognostic biomarker for glioma patients and is associated with poor prognosis. Additionally, SKP2 is closely related to the glioma cell cycle, suggesting that SKP2 may serve as a potential therapeutic target. However, further prospective studies and external cohort validations are needed to confirm its clinical applicability.</p>

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SKP2 protein as a prognostic biomarker for glioma and promotes tumor progression by regulating the cell cycle

  • Lei Guan,
  • Haima Li,
  • Yezu Liu,
  • Jia Ouyang,
  • Changxiang Yan,
  • Feng Liu

摘要

SKP2 (S-phase kinase-associated protein 2) plays an important role in the regulation of the cell cycle, tumorigenesis, progression, and metastasis. However, its functional role in gliomas is currently unclear. This study aimed to investigate the relationship between SKP2 and the progression of gliomas, and its effects on the glioma cell cycle. The relationship between SKP2 expression levels and clinical characteristics of gliomas was explored in our datasets. Kaplan–Meier analysis and COX regression were conducted to evaluate the prognostic role of SKP2. Differentially expressed genes were identified between high and low SKP2 groups. The function and related mechanisms of SKP2 were evaluated based on Gene Ontology and Gene Set Enrichment Analysis. LASSO-Cox was used to screen the variables, and the prediction model was established by nomogram analysis. The effects of SKP2 on the glioma cell cycle were examined in cellular experiments. The SKP2 expression level was positively correlated with adverse clinical features of gliomas, and overall survival with high SKP2 expression was significantly shortened. Gene enrichment analysis showed that the differential genes in the SKP2 high-expression group were mainly enriched in cell cycle and mitosis. In vitro experiments confirmed that silencing of SKP2 arrested the glioma cell cycle at the G1 phase in both U87 and U251 cells. In conclusion, SKP2 may serve as a potential prognostic biomarker for glioma patients and is associated with poor prognosis. Additionally, SKP2 is closely related to the glioma cell cycle, suggesting that SKP2 may serve as a potential therapeutic target. However, further prospective studies and external cohort validations are needed to confirm its clinical applicability.