Aurora B Overexpression Associates with the Thyroid Carcinoma Undifferentiated Phenotype and Is Required for Thyroid Carcinoma Cell Proliferation

Base Sequence Reverse Transcriptase Polymerase Chain Reaction Carcinoma Transplantation, Heterologous Mice, Nude Protein Serine-Threonine Kinases Gene Expression Regulation, Enzymologic 3. Good health Gene Expression Regulation, Neoplastic Mice 03 medical and health sciences Phenotype 0302 clinical medicine Aurora Kinases Cell Line, Tumor Animals Aurora Kinase B Humans Thyroid Neoplasms Cell Division DNA Primers
DOI: 10.1210/jc.2004-1518 Publication Date: 2005-02-08T01:17:00Z
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.
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