title: Overexpression of Aurora-A contributes to malignant development of human esophageal squamous cell carcinoma.
abstract: OBJECTIVE
  Aurora-A/STK15/BTAK, a centrosome-associated oncogenic protein, is implicated in the control of mitosis. Overexpression of Aurora-A has been shown to result in chromosomal aberration and genomic instability. Multiple lines of evidence indicate that Aurora-A induces cell malignant transformation. In the current study, we are interested in investigating the expression of Aurora-A in human esophageal squamous cell carcinoma (ESCC) and characterizing the association of Aurora-A with ESCCmalignant progression.
  
  
  METHODS
  Aurora-A protein expression was examined in 84 ESCC tissues and 81 paired normal adjacent tissues by either immunohistochemistry or Western blot analysis. In addition, a gene-knockdown small interfering RNA technique was used in ESCC cells to investigate whether Aurora-A contributes to the ability of a tumor to grow invasively.
  
  
  RESULTS
  The amount of Aurora-A protein in ESCC was considerably higher than that in normal adjacent tissues. Overexpression of Aurora-A was observed in 57 of 84 (67.5%) ESCC samples. In contrast, <2% of normal adjacent tissue displayed high expression of Aurora-A. Interestingly, overexpression of Aurora-A seemed to correlate with the invasive malignancy of ESCC. Disruption of endogenous Aurora-A using small interfering RNA technique substantially suppressed cell migrating ability.
  
  
  CONCLUSIONS
  The findings presented in this report show that Aurora-A expression is elevated in human esophageal squamous cell carcinoma and is possibly associated with tumor invasion, indicating that overexpression of Aurora-A may contribute to ESCC occurrence and progression.
authors.affiliation: State Key Laboratory of Molecular Oncology , Cancer Institute, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, People's Republic of China.
authors.forename: Tong
authors.initials: T
authors.lastname: Tong
authors.forename: Yali
authors.initials: Y
authors.lastname: Zhong
authors.forename: Jianping
authors.initials: J
authors.lastname: Kong
authors.forename: Lijia
authors.initials: L
authors.lastname: Dong
authors.forename: Yongmei
authors.initials: Y
authors.lastname: Song
authors.forename: Ming
authors.initials: M
authors.lastname: Fu
authors.forename: Zhihua
authors.initials: Z
authors.lastname: Liu
authors.forename: Mingrong
authors.initials: M
authors.lastname: Wang
authors.forename: Liping
authors.initials: L
authors.lastname: Guo
authors.forename: Shixin
authors.initials: S
authors.lastname: Lu
authors.forename: Ming
authors.initials: M
authors.lastname: Wu
authors.forename: Qimin
authors.initials: Q
authors.lastname: Zhan
mesh_terms: D064096:Aurora Kinase A; D064127:Aurora Kinases; D015153:Blotting, Western; D002294:Carcinoma, Squamous Cell / Q000378:metabolism* / Q000473:pathology; D018797:Cell Cycle Proteins; D045744:Cell Line, Tumor; D002465:Cell Movement; D018385:Centrosome / Q000648:ultrastructure; D018450:Disease Progression; D004938:Esophageal Neoplasms / Q000378:metabolism* / Q000473:pathology; D004947:Esophagus / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D008856:Microscopy, Fluorescence; D011494:Protein Kinases / Q000096:biosynthesis* / Q000502:physiology*; D017346:Protein Serine-Threonine Kinases; D034741:RNA, Small Interfering / Q000378:metabolism; D013997:Time Factors; D029867:Xenopus Proteins
chemical_list: D018797:Cell Cycle Proteins; D034741:RNA, Small Interfering; D029867:Xenopus Proteins; D011494:Protein Kinases; C112134:AURKA protein, Xenopus; C576917:AURKA protein, human; D064096:Aurora Kinase A; D064127:Aurora Kinases; D017346:Protein Serine-Threonine Kinases