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

S Duensing, LY Lee, A Duensing… - Proceedings of the …, 2000 - National Acad Sciences
S Duensing, LY Lee, A Duensing, J Basile, S Piboonniyom, S Gonzalez, CP Crum
Proceedings of the National Academy of Sciences, 2000National Acad Sciences
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 …
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.
National Acad Sciences