Abstract:
:Infection by human papillomaviruses (HPV) leads to the formation of benign lesions, warts, and in some cases, cervical cancer. The formation of these lesions is dependent upon increased expression of proangiogenic factors. Angiogenesis is linked to tissue hypoxia through the activity of the oxygen-sensitive hypoxia-inducible factor 1α (HIF-1α). Our studies indicate that the HPV E7 protein enhances HIF-1 transcriptional activity whereas E6 functions to counteract the repressive effects of p53. Both high- and low-risk HPV E7 proteins were found to bind to HIF-1α through a domain located in the N-terminus. Importantly, the ability of E7 to enhance HIF-1 activity mapped to the C-terminus and correlated with the displacement of the histone deacetylases HDAC1, HDAC4, and HDAC7 from HIF-1α by E7. Our findings describe a novel role of the E7 oncoprotein in activating the function of a key transcription factor mediating hypoxic responses by blocking the binding of HDACs.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Bodily JM,Mehta KP,Laimins LAdoi
10.1158/0008-5472.CAN-10-2626subject
Has Abstractpub_date
2011-02-01 00:00:00pages
1187-95issue
3eissn
0008-5472issn
1538-7445pii
0008-5472.CAN-10-2626journal_volume
71pub_type
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