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The human papillomavirus type 16 E6 and E7 oncoproteins cooperate to induce mitotic defects and genomic instability by uncoupling centrosome duplication from the cell division cycle

Duensing, Stefan, Lee, Lily Y., Duensing, Anette, Basile, John, Piboonniyom, Siribang-on, Gonzalez, Sonia, Crum, Christopher P., Münger, Karl·2000·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.170093297
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Abstract

Loss of genomic integrity is a defining feature of many human malignancies, including human papillomavirus (HPV)-associated preinvasive and invasive genital squamous lesions. Here we show that aberrant mitotic spindle pole formation caused by abnormal centrosome numbers represents an important mechanism in accounting for numeric chromosomal alterations in HPV-associated carcinogenesis. Similar to what we found in histopathological specimens, HPV-16 E6 and E7 oncoproteins cooperate to induce abnormal centrosome numbers, aberrant mitotic spindle pole formation, and genomic instability. The low-risk HPV-6 E6 and E7 proteins did not induce such abnormalities. Whereas the HPV-16 E6 oncoprotein has no immediate effects on centrosome numbers, HPV-16 E7 rapidly induces abnormal centrosome duplication. Thus our results suggest a model whereby HPV-16 E7 induces centrosome-related mitotic disturbances that are potentiated by HPV-16 E6.

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Metadata

Authors
Duensing, S., Lee, L. Y., Duensing, A., Basile, J., Piboonniyom, S.-O., Gonzalez, S., Crum, C. P., & Münger, K.
Affiliations
Department of Pathology and Harvard Center for Cancer Biology, Department of Pathology, Solid Tumor Cytogenetics, Brigham and Women's Hospital, and Division of Women's and Perinatal Pathology, Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115
Venue
Proceedings of the National Academy of Sciences
Publisher
National Academy of Sciences
Published
2000-08-15
Volume
97
Issue
18
Pages
10002-10007
ISSN
  • 0027-8424
  • 1091-6490
DOI
10.1073/pnas.170093297
Cited by
397
References
2
Language
en

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