YUNG-MING JENGPeng S.-Y.Lin C.-Y.Hsu H.-C.2020-03-062020-03-0620041078-0432https://www.scopus.com/inward/record.uri?eid=2-s2.0-1642361744&doi=10.1158%2f1078-0432.CCR-1057-03&partnerID=40&md5=b2970064bcfcc3f954373be610aaab80https://scholars.lib.ntu.edu.tw/handle/123456789/473486Purpose: Aurora-A/STK15/BTAK, a centrosome-associated serine/threonine kinase, has been shown to induce chromosomal instability, leading to aneuploidy and cell transformation. The purpose of this study was to investigate the expression and amplification of Aurora-A in hepatocellular carcinoma (HCC). Experimental Design: Aurora-A mRNA levels were measured in 224 HCCs and 199 paired nontumorous liver tissues by reverse transcription-PCR. Aurora-A mRNA and protein levels of 8 were also measured by reverse transcription-PCR and Western blot hybridization in 8 liver cancer cell lines. Amplification of Aurora-A was determined by Southern blot hybridization in 99 cases. Results: Aurora-A was overexpressed in 137 of 224 (61%) RCCs and all 8 of the cell lines. Overexpression of Aurora-A was associated with high-grade (grade II-IV), and high-stage (stage IIIB-IV) tumors, p53 mutation, infrequent β-catenin mutation, and poor outcome. Aurora-A overexpression and p53 mutation acted synergistically toward poor prognosis. Amplification of Aurora-A was detected only in 3 HCCs. Conclusion: The results show that Aurora-A is overexpressed frequently in HCC, and correlated with high grade and high stage, indicating that overexpression of Aurora-A plays a role in the development and progression of HCC.[SDGs]SDG3alpha fetoprotein; aurora A kinase; beta catenin; messenger RNA; protein p53; protein serine threonine kinase; unclassified drug; adolescent; adult; aged; aneuploidy; article; Aurora A gene; cancer cell culture; cancer grading; cancer growth; cancer staging; cancer survival; cell transformation; controlled study; female; gene; gene amplification; gene mutation; gene overexpression; genetic stability; human; human cell; human tissue; liver cell carcinoma; major clinical study; male; priority journal; prognosis; reverse transcription polymerase chain reaction; Southern blotting; tumor suppressor gene; Western blotting; alpha-Fetoproteins; Carcinoma, Hepatocellular; Cell Line, Tumor; Female; Gene Amplification; Gene Expression Regulation, Enzymologic; Gene Expression Regulation, Neoplastic; Genes, p53; Humans; Liver; Liver Neoplasms; Male; Mutation; Neoplasm Staging; Protein-Serine-Threonine Kinases; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Survival Analysisjournal article10.1158/1078-0432.CCR-1057-03150417272-s2.0-1642361744