Aurora B overexpression associates with the thyroid carcinoma undifferentiated phenotype and is required for thyroid carcinoma cell proliferation

R Sorrentino, S Libertini, PL Pallante… - The Journal of …, 2005 - academic.oup.com
R Sorrentino, S Libertini, PL Pallante, G Troncone, L Palombini, V Bavetsias…
The Journal of Clinical Endocrinology & Metabolism, 2005academic.oup.com
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 …
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.
Oxford University Press