Human papillomavirus type 16 E7 oncoprotein-induced abnormal centrosome synthesis is an early event in the evolving malignant phenotype

Genomic instability is a hallmark of malignant growth that frequently involves mitotic defects associated with centrosome abnormalities. However, the question of whether abnormal centrosomes cause genomic instability or develop secondary to other changes has not been conclusively resolved. Here we s...

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Bibliographic Details
Published in:Cancer research (Chicago, Ill.) Ill.), 2001-03, Vol.61 (6), p.2356-2360
Main Authors: DUENSING, Stefan, DUENSING, Anette, CRUM, Christopher P, MÜNGER, Karl
Format: Article
Language:English
Subjects:
AE7 protein
Biological and medical sciences
Cell Nucleus - metabolism
Cell physiology
Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes
Cell Transformation, Viral - physiology
Centrioles - metabolism
Centrosome - metabolism
Centrosome - virology
centrosomes
Fundamental and applied biological sciences. Psychology
Human papillomavirus 16
Humans
Keratinocytes - metabolism
Molecular and cellular biology
Oncogene Proteins, Viral - biosynthesis
Oncogene Proteins, Viral - genetics
Oncogene Proteins, Viral - physiology
oncoproteins
Osteosarcoma - metabolism
Papillomaviridae - genetics
Papillomaviridae - metabolism
Papillomavirus E7 Proteins
Phenotype
Tumor Cells, Cultured
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Summary:Genomic instability is a hallmark of malignant growth that frequently involves mitotic defects associated with centrosome abnormalities. However, the question of whether abnormal centrosomes cause genomic instability or develop secondary to other changes has not been conclusively resolved. Here we show that human papillomavirus (HPV)-16 E7 can induce abnormal centrosome synthesis before the development of extensive nuclear abnormalities. In contrast, expression of HPV-16 E6 is associated with marked nuclear atypia and concomitant accumulation of centrosomes. Our results demonstrate that HPV-16 E7-induced centrosome abnormalities represent an early event during neoplastic progression potentially driving genomic destabilization.
ISSN:0008-5472
1538-7445