Nucleic Acids Research, 1990, Vol. 18, No. 4 763-769
© 1990
MOLECULAR BIOLOGY |
Transcription of the transforming genes of the oncogenic human papillomavirus-16 is stimulated by tumor promotors through AP1 binding sites
Institute of Molecular and Cell Biology, National University of Singapore Kent Ridge, 0511 Singapore
*To whom correspondeoce should be addressed
+Present address: Techmcal University of Darmstadt, Institute of Biochemistry, Petersenstraße 22, 6100 Darms PRO
Received November 21, 1989. Revised January 26, 1990. Accepted January 26, 1990.
The promoter P97 of human papillomavirus-16 (HPV-16) gives rise to transcripts that encode the principal transforming genes of the virus, E6 and E7. The activity of P97 is regulated by a cell-type-specific enhancer, as well as by glucocorticolds and progesterone. We show here, that in CaSki cells, which contain HPV-16 genomes, P97 is also inducible by phorbol esters. Functional analysis of restriction fragments and oligonucleotides of the viral enhancer localizes two phorbol eater response elements on two transcription factor binding sites termed fp4e and fp9e. Sequence comparison, footprint analysis and bandshift competition of the cloned motifs suggest that both fp4e and fp9e are bound by the transcription factor AP1. These AP1 binding sites in HPV-16 and other papillomaviruses may provide a link between cellular oncogenes like jun, fos and possibly ras, whose transcription stimulating activity may lead to an elevated expression of the viral transforming genes E6 and E7.
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