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Human Papillomavirus Type 16 E7 Oncoprotein Can Induce Abnormal Centrosome Duplication through a Mechanism Independent of Inactivation of Retinoblastoma Protein Family Members

Duensing, Stefan, Münger, Karl·2003·Journal of Virology
DOI 10.1128/jvi.77.22.12331-12335.2003
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Abstract

The human papillomavirus type 16 (HPV-16) E7 oncoprotein rapidly induces centrosome duplication errors in primary human cells, thereby increasing the propensity for multipolar mitoses, which can lead to chromosome missegregation and aneuploidy. We analyzed a series of HPV-16 E7 mutants and demonstrate that this biological activity of the E7 oncoprotein is mediated by sequences encompassing the core pRB binding site but is independent of its ability to inactivate the retinoblastoma tumor suppressor protein pRB and the related pocket proteins p107 and p130. In addition, interaction of E7 with the S4 subunit of the 26S proteasome and dysregulation of cdc25A transcription are also dispensable for the induction of centrosome duplication errors. Consistent with these results, expression of HPV-16 E7 induces abnormal centrosome duplication in a cell line that lacks functional pRB and in mouse embryo fibroblasts that are deficient for pRB, p107, and p130. These results demonstrate that the molecular mechanism whereby HPV-16 E7 induces centrosome duplication errors is independent of its ability to inactivate pRB, p107, and p130 or to interact with the S4 proteasome subunit.

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Cited by

Metadata

Authors
Duensing, S., & Münger, K.
Affiliations
Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115
Venue
Journal of Virology
Publisher
American Society for Microbiology
Published
2003-11-15
Volume
77
Issue
22
Pages
12331-12335
ISSN
  • 0022-538X
  • 1098-5514
DOI
10.1128/jvi.77.22.12331-12335.2003
Cited by
91
References
2
Language
en
Licence
journals.asm.org/non-commercial-tdm-license (tdm)

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