title: Aurora B overexpression associates with the thyroid carcinoma undifferentiated phenotype and is required for thyroid carcinoma cell proliferation.
abstract: Alterations in chromosome number (aneuploidy) are common in human neoplasias. Loss of mitotic regulation is believed to induce aneuploidy in cancer cells and act as a driving force during the malignant progression. The serine/theronine protein kinases of aurora family genes play a critical role in the regulation of key cell cycle processes. Aurora B mediates chromosome segregation by ensuring orientation of sister chromatids and overexpression of Aurora B in diploid human cells NHDF (normal human diploid fibroblast) induces multinuclearity. We analyzed Aurora B expression in human thyroid carcinomas. Cell lines originating from different histotypes showed an increase in Aurora B expression. Immunohistochemical analysis of archive samples showed a high expression of Aurora B in anaplastic thyroid carcinomas; conversely, Aurora B expression was not detectable in normal thyroid tissue. Real-time PCR analysis confirmed a strong expression of Aurora B in anaplastic thyroid carcinomas. The block of Aurora B expression induced by RNA interference or by using an inhibitor of Aurora kinase activity significantly reduced the growth of thyroid anaplastic carcinoma cells.
authors.affiliation: Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università Federico II, via S. Pansini 5, 80131 Napoli, Italy.
authors.forename: Rosanna
authors.initials: R
authors.lastname: Sorrentino
authors.forename: Silvana
authors.initials: S
authors.lastname: Libertini
authors.forename: Pier Lorenzo
authors.initials: PL
authors.lastname: Pallante
authors.forename: Giancarlo
authors.initials: G
authors.lastname: Troncone
authors.forename: Lucio
authors.initials: L
authors.lastname: Palombini
authors.forename: Vassilios
authors.initials: V
authors.lastname: Bavetsias
authors.forename: Daniela
authors.initials: D
authors.lastname: Spalletti-Cernia
authors.forename: Paolo
authors.initials: P
authors.lastname: Laccetti
authors.forename: Spiros
authors.initials: S
authors.lastname: Linardopoulos
authors.forename: Paolo
authors.initials: P
authors.lastname: Chieffi
authors.forename: Alfredo
authors.initials: A
authors.lastname: Fusco
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Portella
mesh_terms: D000818:Animals; D064107:Aurora Kinase B; D064127:Aurora Kinases; D001483:Base Sequence; D002277:Carcinoma / Q000201:enzymology / Q000235:genetics / Q000473:pathology; D002455:Cell Division; D045744:Cell Line, Tumor; D017931:DNA Primers; D015971:Gene Expression Regulation, Enzymologic; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D051379:Mice; D008819:Mice, Nude; D010641:Phenotype; D017346:Protein Serine-Threonine Kinases / Q000235:genetics*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013964:Thyroid Neoplasms / Q000201:enzymology / Q000235:genetics* / Q000473:pathology; D014183:Transplantation, Heterologous
chemical_list: D017931:DNA Primers; C576921:AURKB protein, human; C576924:Aurkb protein, mouse; D064107:Aurora Kinase B; D064127:Aurora Kinases; D017346:Protein Serine-Threonine Kinases