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
AUTHORS (12)
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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