Journal
CARCINOGENESIS
Volume 30, Issue 5, Pages 753-757Publisher
OXFORD UNIV PRESS
DOI: 10.1093/carcin/bgp066
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Funding
- Korea Research Foundation [KRF-2007-313-E00380]
- Brain Korea 21 project for Medicine, Dentistry and Pharmacy
- National Research Foundation of Korea [2007-313-E00380] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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The human papillomavirus (HPV) E6 and E7 oncoproteins play important roles in cervical carcinogenesis through multiple mechanisms, including upregulation of cyclooxygenase-2 (COX-2), which has been shown to be involved in both carcinogenesis and cancer progression. To explore the role of E5 in cervical carcinogenesis, we herein investigated the effect of HPV 16 E5 on COX-2 expression. Our results revealed that E5 induced COX-2 expression through the epidermal growth factor receptor-signaling pathway, with nuclear factor-kappaB (NF-kappa B) and activator protein-1 (AP-1) acting as critical factors in E5-induced COX-2 expression. NF-kappa B inhibition blocked COX-2 expression more potently than inhibition of AP-1. Our findings collectively suggest that the HPV 16 E5 oncoprotein mediates cervical carcinogenesis at least in part via upregulation of COX-2 expression through NF-kappa B and AP-1, with NF-kappa B playing a larger role.
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