Journal of Neuro-Oncology

, Volume 67, Issue 1–2, pp 53–64 | Cite as

High Expression of Aurora-B/Aurora and Ipl1-Like Midbody-Associated Protein (AIM-1) in Astrocytomas

  • Kasumi Araki
  • Kazuhiko Nozaki
  • Tetsuya Ueba
  • Masaaki Tatsuka
  • Nobuo Hashimoto


Objective: Impaired regulation of Aurora-B/AIM-1 expression in human cells causes chromosomal abnormality and instability, and recent observations of high expression but not mutation of Aurora-B/AIM-1 in human cancers imply that Aurora-B/AIM-1 might be a candidate molecule for cancer progression. We analyzed the effects of modification of Aurora-B/AIM-1 expression on the growth of a human glioma cell line and the expression of Aurora-B/AIM-1 in astrocytomas.

Methods: A glioma cell line, U251MG was transfected with wild type (WT) of Aurora-B/AIM-1 or kinase-inactive mutant of Aurora-B/AIM-1 in order to test the effects of overexpression of WT or kinase-inactive Aurora-B/AIM-1 on cell morphology and cell growth. Brain tissue samples were obtained during surgery and processed for reverse transcription-polymerase chain reaction, immunofluorescence in order to analyze the expression of Aurora-B/AIM-1 mRNA and protein.

Results: Exogenous overexpression of WT of Aurora-B/AIM-1 in cultured cells of U251MG produced multinuclearity and increased ploidy, and inhibited the growth of tumor cells. Exogenous overexpression of kinase-inactive Aurora-B/AIM-1 in a human glioma cell line also suppressed the tumor cell growth without affecting ploidy. Aurora-B/AIM-1 was highly expressed in astrocytomas and U251MG, and mRNA and protein levels of Aurora-B/AIM-1 in tumor tissues well correlated with their histological malignancy (World Health Organization grading). Survival time also negatively correlated with the levels of Aurora-B/AIM-1 mRNA in tumor samples.

Conclusion: Aurora-B/AIM-1 was highly expressed in high-grade gliomas and its expression was well correlated with histological malignancy and clinical outcomes. The modification of the level of Aurora-B/AIM-1 expression might be a new target for glioma therapy.

astrocytomas Aurora-B/AIM-1 central nervous system ploidy U251MG 


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Copyright information

© Kluwer Academic Publishers 2004

Authors and Affiliations

  • Kasumi Araki
    • 1
  • Kazuhiko Nozaki
    • 1
  • Tetsuya Ueba
    • 1
  • Masaaki Tatsuka
    • 2
  • Nobuo Hashimoto
    • 1
  1. 1.Department of NeurosurgeryKyoto University Graduate School of MedicineKyotoJapan
  2. 2.Department of Molecular Radiobiology, Research Institution for Radiation Biology and MedicineHiroshima UniversityHiroshimaJapan

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