Differential cell cycle regulation by low- and high-risk human papillomaviruses in low-grade squamous intraepithelial lesions of the cervix

• Published in: Cancer research (Chicago, Ill.) Vol. 58; no. 14; pp. 2941 - 2945
• Main Authors: SOUTHERN, S. A, HERRINGTON, C. S
• Format: Journal Article
• Language: English
• Published: Philadelphia, PA American Association for Cancer Research 15.07.1998
• Subjects: Biological and medical sciences; Cell Cycle; Cervical Intraepithelial Neoplasia - metabolism; Cervical Intraepithelial Neoplasia - pathology; Cervical Intraepithelial Neoplasia - virology; Chromosome Aberrations; Chromosome Disorders; Cyclin D1 - metabolism; Epithelium - metabolism; Epithelium - virology; Female; Female genital diseases; Gynecology. Andrology. Obstetrics; Human papillomavirus; Humans; Medical sciences; Papillomaviridae - classification; Papillomaviridae - physiology; Papillomavirus Infections - metabolism; Papillomavirus Infections - pathology; Tumor Virus Infections - metabolism; Tumor Virus Infections - pathology; Tumors; Uterine Cervical Neoplasms - metabolism; Uterine Cervical Neoplasms - pathology; Uterine Cervical Neoplasms - virology; Warts - metabolism; Warts - virology; Chromosomal aberration; Human; Gene product; Tumoral tissue; Cyclin; Aneuploidy; Tetrasomy; Papovaviridae; Uterine cervix; Malignant tumor; Gene expression; Female genital diseases; Papillomavirus; Virus; Human papillomavirus; Low malignancy; C-Onc gene; Cell cycle; Genetics; Abnormal chromosome; Uterine cervix diseases
• ISSN: 0008-5472; 1538-7445

In this study, we have demonstrated the overexpression of cyclin D1 protein in 24 (92%) of 26 low-grade squamous intraepithelial lesions infected with low-risk human papillomaviruses (HPV 6, 11, 42, 43, and 44) and the absence of cyclin D1 expression in 25 (87%) of 29 lesions infected with high-risk HPVs (HPV 16, 18, 31, 33, 39, 45, 51, 52, 56, 58, and 66). The expression of cyclins E, A, and B proteins was increased in both low-risk and high-risk HPV infections. Tetrasomy of chromosomes 1, 3, 11, 17, 18, and X was present in nine lesions, all of which were infected with high-risk HPVs, but was not related to the pattern of cyclin expression. These data provide in vivo evidence that low- and high-risk HPV types alter cell cycle control by different mechanisms and that cell cycle checkpoint abnormalities are induced by high-risk, but not low-risk, HPV infection.