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Opposite regulation of the HPV 20‐URR and HPV 27‐URR promoters by ultraviolet irradiation and cytokines

Opposite regulation of the HPV 20‐URR and HPV 27‐URR promoters by ultraviolet irradiation and... Epidemiological evidence implicates ultraviolet radiation and genetic changes (e.g., p53 mutations) as important factors in the etiology of nonmelanoma skin cancer. Little is known about a possible role of cutaneous papillomaviruses in these tumors. We previously reported both positive and negative regulation of the promoter activity of a number of HPV types by UV irradiation. To determine the underlying mechanism, we examined the influence of pro‐inflammatory cytokines and MAP‐kinases induced by UV irradiation by transfecting the HPV 20‐URR and the HPV 27‐URR into the RKO, HaCaT and H1299 cell lines expressing wild‐type or mutated p53 or lacking p53, respectively. IL‐1α, IL‐1β, IL‐6, IL‐17, TNF‐α, as well as interferon‐α, ‐β and ‐γ activated the promoter in the HPV 20‐URR but inhibited the HPV 27‐URR promoter. The effect of IL‐1α and UV light was abolished by the addition of IL‐1 receptor antagonist. UV irradiation induced a prolonged activation of JNK in HaCaT and H1299 but not in RKO cells, and its dephosphorylation was enhanced in the presence of p53 and the HPV‐URRs. © 2001 Wiley‐Liss, Inc. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png International Journal of Cancer Wiley

Opposite regulation of the HPV 20‐URR and HPV 27‐URR promoters by ultraviolet irradiation and cytokines

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References (46)

Publisher
Wiley
Copyright
Copyright © 2001 Wiley Subscription Services
ISSN
0020-7136
eISSN
1097-0215
DOI
10.1002/1097-0215(200002)9999:9999<::AID-IJC1129>3.0.CO;2-B
Publisher site
See Article on Publisher Site

Abstract

Epidemiological evidence implicates ultraviolet radiation and genetic changes (e.g., p53 mutations) as important factors in the etiology of nonmelanoma skin cancer. Little is known about a possible role of cutaneous papillomaviruses in these tumors. We previously reported both positive and negative regulation of the promoter activity of a number of HPV types by UV irradiation. To determine the underlying mechanism, we examined the influence of pro‐inflammatory cytokines and MAP‐kinases induced by UV irradiation by transfecting the HPV 20‐URR and the HPV 27‐URR into the RKO, HaCaT and H1299 cell lines expressing wild‐type or mutated p53 or lacking p53, respectively. IL‐1α, IL‐1β, IL‐6, IL‐17, TNF‐α, as well as interferon‐α, ‐β and ‐γ activated the promoter in the HPV 20‐URR but inhibited the HPV 27‐URR promoter. The effect of IL‐1α and UV light was abolished by the addition of IL‐1 receptor antagonist. UV irradiation induced a prolonged activation of JNK in HaCaT and H1299 but not in RKO cells, and its dephosphorylation was enhanced in the presence of p53 and the HPV‐URRs. © 2001 Wiley‐Liss, Inc.

Journal

International Journal of CancerWiley

Published: Jan 15, 2001

Keywords: ; ;

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