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CCAAT/enhancer-binding protein represses human papillomavirus 11 upstream regulatory region expression through a promoter-proximal YY1-binding site

¹ Northshore-Long Island Jewish Research Institute, 350 Community Drive, Manhasset, NY 11030, USA
² Department of Otolaryngology, Long Island Jewish Medical Center, Long Island Campus of Albert Einstein College of Medicine, New Hyde Park, NY 11040, USA

Correspondence
Walter M. Ralph, Jr
wralphmd{at}optonline.net

CCAAT/enhancer-binding protein (C/EBP) can function as a repressor or as an activator of human papillomavirus (HPV) gene expression, depending on which cell type the experiments are conducted. In this report, it was shown that within primary human foreskin keratinocyte cells (HFK) the activity of C/EBP can be switched from that of a repressor of HPV11 expression to an activator by mutating a single promoter-proximal consensus YY1-binding site within the HPV11 upstream regulatory region (URR). It was shown that in HFK cells, exogenous expression of C/EBP significantly activates the expression of mutant HPV11 URR reporter plasmids that contain deletions which overlap a 127 bp region (–269 to –142). Inclusive in this region are binding sites for multiple transcription factors, including AP1, YY1 and C/EBP. Only mutation of the YY1 site resulted in the switch in phenotype, indicating that C/EBP represses HPV11 expression in these cells via YY1 binding. The level of YY1 activity was also measured in HFK cells transfected with a C/EBP expression plasmid and a significant increase in YY1 activity as compared with mock-transfected cells was found. C33A cells, which exhibit activation of wild-type HPV11 gene expression with exogenous C/EBP co-expression, failed to demonstrate C/EBP-induced YY1 activation. It was concluded that in HFK cells, exogenous C/EBP induces the activity of YY1, which, in turn, can repress HPV11 URR expression through the promoter-proximal YY1-binding site.