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CCNA2 and NEK2 regulate glioblastoma progression by targeting the cell cycle

  • Authors:
    • Hao-Yu Zhou
    • Yi-Chang Wang
    • Tuo Wang
    • Wei Wu
    • Yi-Yang Cao
    • Bei-Chen Zhang
    • Mao-De Wang
    • Ping Mao
  • View Affiliations / Copyright

    Affiliations: Department of Neurosurgery, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China
    Copyright: © Zhou et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 206
    |
    Published online on: March 13, 2024
       https://doi.org/10.3892/ol.2024.14339
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Abstract

Glioblastoma (GBM) is characterized by significant heterogeneity, leading to poor survival outcomes for patients, despite the implementation of comprehensive treatment strategies. The roles of cyclin A2 (CCNA2) and NIMA related kinase 2 (NEK2) have been extensively studied in numerous cancers, but their specific functions in GBM remain to be elucidated. The present study aimed to investigate the potential molecular mechanisms of CCNA2 and NEK2 in GBM. CCNA2 and NEK2 expression and prognosis in glioma were evaluated by bioinformatics methods. In addition, the distribution of CCNA2 and NEK2 expression in GBM subsets was determined using pseudo‑time analysis and tricycle position of single‑cell sequencing. Gene Expression Omnibus and Kyoto Encyclopedia of Genes and Genome databases were employed and enrichment analyses were conducted to investigate potential signaling pathways in GBM subsets and a nomogram was established to predict 1‑, 2‑ and 3‑year overall survival probability in GBM. CCNA2 and NEK2 expression levels were further validated by western blot analysis and immunohistochemical staining in GBM samples. High expression of CCNA2 and NEK2 in glioma indicates poor clinical outcomes. Single‑cell sequencing of GBM revealed that these genes were upregulated in a subset of positive neural progenitor cells (P‑NPCs), which showed significant proliferation and progression properties and may activate G2M checkpoint pathways. A comprehensive nomogram predicts 1‑, 2‑ and 3‑year overall survival probability in GBM by considering P‑NPCs, age, chemotherapy and radiotherapy scores. CCNA2 and NEK2 regulate glioblastoma progression by targeting the cell cycle, thus indicating the potential of novel therapy directed to CCNA2 and NEK2 in GBM.
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Copy and paste a formatted citation
Spandidos Publications style
Zhou H, Wang Y, Wang T, Wu W, Cao Y, Zhang B, Wang M and Mao P: CCNA2 and NEK2 regulate glioblastoma progression by targeting the cell cycle. Oncol Lett 27: 206, 2024.
APA
Zhou, H., Wang, Y., Wang, T., Wu, W., Cao, Y., Zhang, B. ... Mao, P. (2024). CCNA2 and NEK2 regulate glioblastoma progression by targeting the cell cycle. Oncology Letters, 27, 206. https://doi.org/10.3892/ol.2024.14339
MLA
Zhou, H., Wang, Y., Wang, T., Wu, W., Cao, Y., Zhang, B., Wang, M., Mao, P."CCNA2 and NEK2 regulate glioblastoma progression by targeting the cell cycle". Oncology Letters 27.5 (2024): 206.
Chicago
Zhou, H., Wang, Y., Wang, T., Wu, W., Cao, Y., Zhang, B., Wang, M., Mao, P."CCNA2 and NEK2 regulate glioblastoma progression by targeting the cell cycle". Oncology Letters 27, no. 5 (2024): 206. https://doi.org/10.3892/ol.2024.14339
Copy and paste a formatted citation
x
Spandidos Publications style
Zhou H, Wang Y, Wang T, Wu W, Cao Y, Zhang B, Wang M and Mao P: CCNA2 and NEK2 regulate glioblastoma progression by targeting the cell cycle. Oncol Lett 27: 206, 2024.
APA
Zhou, H., Wang, Y., Wang, T., Wu, W., Cao, Y., Zhang, B. ... Mao, P. (2024). CCNA2 and NEK2 regulate glioblastoma progression by targeting the cell cycle. Oncology Letters, 27, 206. https://doi.org/10.3892/ol.2024.14339
MLA
Zhou, H., Wang, Y., Wang, T., Wu, W., Cao, Y., Zhang, B., Wang, M., Mao, P."CCNA2 and NEK2 regulate glioblastoma progression by targeting the cell cycle". Oncology Letters 27.5 (2024): 206.
Chicago
Zhou, H., Wang, Y., Wang, T., Wu, W., Cao, Y., Zhang, B., Wang, M., Mao, P."CCNA2 and NEK2 regulate glioblastoma progression by targeting the cell cycle". Oncology Letters 27, no. 5 (2024): 206. https://doi.org/10.3892/ol.2024.14339
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