title: High expression of Aurora-B/Aurora and Ipll-like midbody-associated protein (AIM-1) in astrocytomas.
abstract: 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Neurosurgery, Kyoto University Graduate School of Medicine, Japan.
authors.forename: Kasumi
authors.initials: K
authors.lastname: Araki
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Nozaki
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Ueba
authors.forename: Masaaki
authors.initials: M
authors.lastname: Tatsuka
authors.forename: Nobuo
authors.initials: N
authors.lastname: Hashimoto
mesh_terms: D000328:Adult; D000368:Aged; D001254:Astrocytoma / Q000378:metabolism* / Q000401:mortality / Q000473:pathology; D064107:Aurora Kinase B; D064127:Aurora Kinases; D014408:Biomarkers, Tumor; D015153:Blotting, Western; D001932:Brain Neoplasms / Q000378:metabolism* / Q000401:mortality / Q000473:pathology; D045744:Cell Line, Tumor; D003459:Crystallins; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008565:Membrane Proteins; D026901:Membrane Transport Proteins / Q000096:biosynthesis*; D008875:Middle Aged; D011379:Prognosis; D017346:Protein Serine-Threonine Kinases / Q000096:biosynthesis*; D012333:RNA, Messenger / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D014408:Biomarkers, Tumor; C105445:CRYBG1 protein, human; D003459:Crystallins; D008565:Membrane Proteins; D026901:Membrane Transport Proteins; D012333:RNA, Messenger; C576921:AURKB protein, human; D064107:Aurora Kinase B; D064127:Aurora Kinases; D017346:Protein Serine-Threonine Kinases