期刊
ENVIRONMENTAL AND MOLECULAR MUTAGENESIS
卷 50, 期 8, 页码 741-747出版社
WILEY
DOI: 10.1002/em.20478
关键词
HPV; centrosome; chromosomal instability; cancer
资金
- Public Health Service [NIH/NCI R01 CA112598]
- American Cancer Society [RSG-07-075-01]
- Susan G. Komen for the Cure Foundation
- Pittsburgh Foundation
- Pennsylvania Department of Health
- NATIONAL CANCER INSTITUTE [R01CA112598] Funding Source: NIH RePORTER
Centrosome aberrations are a frequent finding in human tumors. However, very little is known about the molecular mechanisms leading to disruption of centrosome duplication control and the functional consequences of aberrant centrosome numbers. The high-risk human papillomavirus Type 16 (HPV-16) E6 and E7 oncoproteins are overexpressed in HPV-associated malignancies of the anogenital tract and have been instrumental in delineating different pathways of centrosome amplification. Whereas the E6 oncoprotein was found to provoke centrosome accumulation, the HPV-16 E7 oncoprotein triggers a genuine disruption of the centrosome duplication cycle. Importantly, the E7 oncoprotein can rapidly cause centrosome overduplication through a pathway that involves the concurrent formation of multiple daughters at single maternal centrioles (centriole flowers). Several lines of evidence suggest that cyclin E/CDK2 complexes and Polo-like kinase 4 (PLK4) are crucial players in this process. These findings underscore that the HPV-16 E7 oncoprotein is a unique tool to dissect normal and abnormal centriole biogenesis and the underlying molecular circuitry. Environ. Mal. Mutagen. 50:741-747, 2009. (C) 2009 Wiley-Liss, Inc.
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