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Expression of Concern: Aurora B expression in post‐puberal testicular germ cell tumours
Author(s) -
Esposito Francesco,
Libertini Silvana,
Franco Renato,
Abagnale Antonella,
Marra Luigi,
Portella Giuseppe,
Chieffi Paolo
Publication year - 2009
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.21875
Subject(s) - aurora b kinase , biology , germ cell , mitosis , yolk sac , aurora inhibitor , immunohistochemistry , seminoma , cancer research , cytokinesis , cell cycle , microbiology and biotechnology , cell division , cell , embryo , immunology , genetics , gene , chemotherapy
Abstract Aurora/Ipl1‐related kinases are a conserved family of proteins that are essential for the regulation of chromosome segregation and cytokinesis during mitosis. Aberrant expression and activity of these kinases occur in a wide range of human tumours and have been implicated in mechanisms leading to mitotic spindle aberrations, aneuploidy, and genomic instability. Previous studies of our group have shown that Aurora B expression is restricted to specific germinal cells. In this study, we have evaluated by immunohistochemical analysis Aurora B expression in post‐puberal testicular germ cell tumours (22 seminomas, 2 teratomas, 15 embryonal carcinomas, 5 mixed germinal tumours with a prominent yolk sac tumour component and 1 choriocarcinoma). The Aurora B protein expression was detected in all intratubular germ cell tumours, seminomas and embryonal carcinomas analysed but not in teratomas and yolk sac carcinomas. The immunohistochemical data were further confirmed by Western blot analysis. In addition, the kinase Aurora B was vigorously expressed in GC‐1 cells line derived from murine spermatogonia. The block of Aurora B function induced by a pharmacological inhibitor significantly reduced the growth of GC‐1 cells suggesting that Aurora B is a potential therapeutic target. J. Cell. Physiol. 221: 435–439, 2009. © 2009 Wiley‐Liss, Inc.