Transcriptional regulation of the human papillomavirus-16 E6-E7 promoter by a keratinocyte-dependent enhancer, and by viral E2 trans-activator and repressor gene products: implications for cervical carcinogenesis

T P Cripe; T H Haugen; J P Turk; F Tabatabai; P G Schmid; M Dürst; L Gissmann; A Roman; L P Turek

doi:10.1002/j.1460-2075.1987.tb02709.x

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Transcriptional regulation of the human papillomavirus-16 E6-E7 promoter by a keratinocyte-dependent enhancer, and by viral E2 trans-activator and repressor gene products: implications for cervical carcinogenesis

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Transcriptional regulation of the human papillomavirus-16 E6-E7 promoter by a keratinocyte-dependent enhancer, and by viral E2 trans-activator and repressor gene products: implications for cervical carcinogenesis

T P Cripe, T H Haugen, J P Turk, F Tabatabai, P G Schmid, M Dürst, L Gissmann, A Roman and L P Turek

The EMBO journal, Vol.6(12), pp.3745-3753

12/01/1987

DOI: 10.1002/j.1460-2075.1987.tb02709.x

PMID: 2448139

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Abstract

The transcriptional promoter of the candidate E6-E7 transforming gene region of human papillomavirus (HPV)-16 (P97) was active in transiently transfected cervical carcinoma cells when linked to the HSV-1 tk or bacterial cat genes. Sequences 5' to P97 contain a short enhancer element responding to cellular factor(s) in uninfected human foreskin keratinocytes and in cervical carcinoma cells, but not in human or animal fibroblasts. The E2 trans-activator products of HPV-16 or of the related bovine papillomavirus (BPV)-1 further elevated HPV-16-driven transcripts in co-transfections, and required the presence of E2-binding ACC(N)6GGT cores in cis. A 'short E2' C-terminal repressor gene product (sE2) of HPV-16 or the BPV-1 sE2 repressor not only inhibited viral E2 trans-activation, but also suppressed enhancer response to keratinocytic factors. Suppression by the sE2 products was abolished by deletion of the E2-binding cores in cis or by a mutation in the sE2 DNA binding domain. The keratinocyte-dependent enhancer is likely to contribute to the epithelial cell tropism of HPV-16, and may direct persistent E6-E7 gene transcription in response to cellular factors in cervical carcinoma cells in which the viral E2 genes are inactive.

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Title: Subtitle: Transcriptional regulation of the human papillomavirus-16 E6-E7 promoter by a keratinocyte-dependent enhancer, and by viral E2 trans-activator and repressor gene products: implications for cervical carcinogenesis
Creators: T P Cripe - Department of Pathology, Veterans Administration Medical Center, Iowa City, IA 52242
T H Haugen - Department of Pathology, Veterans Administration Medical Center, Iowa City, IA 52242
J P Turk - Department of Pathology, Veterans Administration Medical Center, Iowa City, IA 52242
F Tabatabai - Department of Pathology, Veterans Administration Medical Center, Iowa City, IA 52242
P G Schmid - Department of Pathology, Veterans Administration Medical Center, Iowa City, IA 52242
M Dürst - Department of Pathology, Veterans Administration Medical Center, Iowa City, IA 52242
L Gissmann - Department of Pathology, Veterans Administration Medical Center, Iowa City, IA 52242
A Roman - Department of Pathology, Veterans Administration Medical Center, Iowa City, IA 52242
L P Turek - Department of Pathology, Veterans Administration Medical Center, Iowa City, IA 52242
Resource Type: Journal article
Publication Details: The EMBO journal, Vol.6(12), pp.3745-3753
DOI: 10.1002/j.1460-2075.1987.tb02709.x
PMID: 2448139
NLM abbreviation: EMBO J
ISSN: 0261-4189
eISSN: 1460-2075
Language: English
Date published: 12/01/1987
Academic Unit: Pathology; Cardiovascular Medicine; Internal Medicine
Record Identifier: 9984048000002771

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