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Effects of human papillomavirus (HPV) type 16 oncoproteins on the expression of involucrin in human keratinocytes

DOI: 10.1186/1743-422x-9-36

Keywords: HPV 16, Oncogenes, Keratinocyte differentiation, Involucrin

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Abstract:

The differentiation of HFK cells by serum and high calcium significantly increased both the mRNA and the protein levels of IVL. The E6 and E7 oncoproteins of HPV16 together caused strong down-regulation of IVL mRNA and protein both in proliferating and in differentiating HFK cells. To study the effects of HPV oncogenes on the IVL promoter, we made transient transfection assays and luciferase tests and found that HPV 16 E6 but not E7 repressed IVL promoter activity in proliferating HFK cells. The inhibitory effect of HPV 16 E6 on the human IVL promoter could be localised to the proximal regulatory region (PRR) of the gene.These results suggest that the down-regulation of IVL promoter activity by HPV 16 E6 significantly contribute to the inhibition of endogenous IVL expression by the HPV 16 oncoproteins. In contrast, the down-regulation of endogenous IVL expression by HPV16 E7 is probably not caused by a direct and specific effect of E7 on the IVL promoter.Papillomaviruses are small DNA viruses, with a circular double-stranded DNA genome of about 8 kbp length [1]. Over 100 human papillomavirus (HPV) types have been identified until now, of which about 40 is able to infect the genital mucosa [2]. Low-risk HPV types (HPV 6, 11, 42) are mainly found in benign genital lesions (condyloma acuminatum) or low grade cervical dysplasias, while high-risk or oncogenic genital types (HPV 16, 18, and others) are causally linked to the development of cervical cancer [3].The E6 and E7 oncoproteins of high-risk HPVs are responsible for the transforming activity of the virus [4]. High-risk HPV E6 induces the degradation of the p53 tumour suppressor protein through the ubiquitin-proteosome pathway [5]. In addition, HPV E6 is able to bind several other cellular proteins, some of which can mediate transforming activity independently from the p53 pathway [5]. High-risk HPV E7 is able to bind to the pRB (retinoblastoma) tumour suppressor protein, resulting in the functional inactivation and

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