Open Access
,
volume 97
,
issue 18
,
pages 10002-10007
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
Stefan Duensing
1
,
Lily Y Lee
1
,
Anette Duensing
1
,
John Basile
1
,
Siribang-on Piboonniyom
1
,
Sonia González
1
,
Christopher P. Crum
1
,
Karl Münger
1
Publication type: Journal Article
Publication date: 2000-08-15
scimago Q1
wos Q1
SJR: 3.414
CiteScore: 16.5
Impact factor: 9.1
ISSN: 00278424, 10916490
PubMed ID:
10944189
Multidisciplinary
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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Metrics
384
Total citations:
384
Citations from 2024:
21
(5.46%)
Cite this
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GOST
Copy
Duensing S. et al. 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 // Proceedings of the National Academy of Sciences of the United States of America. 2000. Vol. 97. No. 18. pp. 10002-10007.
GOST all authors (up to 50)
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Duensing S., Lee L. Y., Duensing A., Basile J., Piboonniyom S., González S., Crum C. P., Münger K. 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 // Proceedings of the National Academy of Sciences of the United States of America. 2000. Vol. 97. No. 18. pp. 10002-10007.
Cite this
RIS
Copy
TY - JOUR
DO - 10.1073/pnas.170093297
UR - https://doi.org/10.1073/pnas.170093297
TI - 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
T2 - Proceedings of the National Academy of Sciences of the United States of America
AU - Duensing, Stefan
AU - Lee, Lily Y
AU - Duensing, Anette
AU - Basile, John
AU - Piboonniyom, Siribang-on
AU - González, Sonia
AU - Crum, Christopher P.
AU - Münger, Karl
PY - 2000
DA - 2000/08/15
PB - Proceedings of the National Academy of Sciences (PNAS)
SP - 10002-10007
IS - 18
VL - 97
PMID - 10944189
SN - 0027-8424
SN - 1091-6490
ER -
Cite this
BibTex (up to 50 authors)
Copy
@article{2000_Duensing,
author = {Stefan Duensing and Lily Y Lee and Anette Duensing and John Basile and Siribang-on Piboonniyom and Sonia González and Christopher P. Crum and Karl Münger},
title = {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},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
year = {2000},
volume = {97},
publisher = {Proceedings of the National Academy of Sciences (PNAS)},
month = {aug},
url = {https://doi.org/10.1073/pnas.170093297},
number = {18},
pages = {10002--10007},
doi = {10.1073/pnas.170093297}
}
Cite this
MLA
Copy
Duensing, Stefan, et al. “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.” Proceedings of the National Academy of Sciences of the United States of America, vol. 97, no. 18, Aug. 2000, pp. 10002-10007. https://doi.org/10.1073/pnas.170093297.