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The FOXM1/BUB1B signaling pathway is essential for the tumorigenicity and radioresistance of glioblastoma

  • Authors:
    • Qing Ma
    • Yanmei Liu
    • Liang Shang
    • Jiao Yu
    • Qiumin Qu
  • View Affiliations / Copyright

    Affiliations: The Third Affiliated Hospital, Medical School of Xi'an Jiaotong University, Xi'an, Shaanxi 710068, P.R. China, The Department of West Yard Ward 2 (Geriatrics), Shaanxi Provincial People's Hospital, Xi'an, Shaanxi 710068, P.R. China, Department of Radiotherapy, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi 710068, P.R. China, Department of Internal Neurology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China
    Copyright: © Ma et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 3367-3375
    |
    Published online on: October 12, 2017
       https://doi.org/10.3892/or.2017.6032
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Abstract

Accumulating evidence indicates that mitotic checkpoint serine/threonine kinase B (BUB1B) plays a critical role in multiple types of cancer. However, the biological function and molecular regulatory mechanism of BUB1B in glioblastoma (GBM) remain unclear. In the present study, we identified that BUB1B expression was enriched in GBM tumors and was functionally required for tumor proliferation both in vitro and in vivo. Clinically, BUB1B expression was associated with poor prognosis in GBM patients and BUB1B‑dependent radioresistance in GBM was decreased by targeting BUB1B via shRNAs. Mechanistically, forkhead box protein M1 (FOXM1) transcriptionally regulated BUB1B expression by binding to and then activating the BUB1B promoter. Therapeutically, we found that FOXM1 inhibitor attenuated tumorigenesis and radioresistance of GBM both in vitro and in vivo. Altogether, BUB1B promotes tumor proliferation and induces radioresistance in GBM, indicating that BUB1B could be a potential therapeutic target for GBM.
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Copy and paste a formatted citation
Spandidos Publications style
Ma Q, Liu Y, Shang L, Yu J and Qu Q: The FOXM1/BUB1B signaling pathway is essential for the tumorigenicity and radioresistance of glioblastoma. Oncol Rep 38: 3367-3375, 2017.
APA
Ma, Q., Liu, Y., Shang, L., Yu, J., & Qu, Q. (2017). The FOXM1/BUB1B signaling pathway is essential for the tumorigenicity and radioresistance of glioblastoma. Oncology Reports, 38, 3367-3375. https://doi.org/10.3892/or.2017.6032
MLA
Ma, Q., Liu, Y., Shang, L., Yu, J., Qu, Q."The FOXM1/BUB1B signaling pathway is essential for the tumorigenicity and radioresistance of glioblastoma". Oncology Reports 38.6 (2017): 3367-3375.
Chicago
Ma, Q., Liu, Y., Shang, L., Yu, J., Qu, Q."The FOXM1/BUB1B signaling pathway is essential for the tumorigenicity and radioresistance of glioblastoma". Oncology Reports 38, no. 6 (2017): 3367-3375. https://doi.org/10.3892/or.2017.6032
Copy and paste a formatted citation
x
Spandidos Publications style
Ma Q, Liu Y, Shang L, Yu J and Qu Q: The FOXM1/BUB1B signaling pathway is essential for the tumorigenicity and radioresistance of glioblastoma. Oncol Rep 38: 3367-3375, 2017.
APA
Ma, Q., Liu, Y., Shang, L., Yu, J., & Qu, Q. (2017). The FOXM1/BUB1B signaling pathway is essential for the tumorigenicity and radioresistance of glioblastoma. Oncology Reports, 38, 3367-3375. https://doi.org/10.3892/or.2017.6032
MLA
Ma, Q., Liu, Y., Shang, L., Yu, J., Qu, Q."The FOXM1/BUB1B signaling pathway is essential for the tumorigenicity and radioresistance of glioblastoma". Oncology Reports 38.6 (2017): 3367-3375.
Chicago
Ma, Q., Liu, Y., Shang, L., Yu, J., Qu, Q."The FOXM1/BUB1B signaling pathway is essential for the tumorigenicity and radioresistance of glioblastoma". Oncology Reports 38, no. 6 (2017): 3367-3375. https://doi.org/10.3892/or.2017.6032
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