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Carcinogenesis Advance Access originally published online on June 19, 2008
Carcinogenesis 2008 29(7):1441-1447; doi:10.1093/carcin/bgn145
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© The Author 2008. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Silencing of E7 oncogene restores functional E-cadherin expression in human papillomavirus 16-transformed keratinocytes

Jean-Hubert D. Caberg*,{dagger}, Pascale M. Hubert{dagger}, Dominique Y. Begon, Michael F. Herfs, Patrick J. Roncarati, Jacques J. Boniver and Philippe O. Delvenne

Department of Pathology, Groupe Interdisciplinaire de Génoprotéomique Appliquée-Cancer, B23, University of Liege, Centre Hospitalier Universitaire Sart Tilman, 4000 Liege, Belgium

* To whom correspondence should be addressed. Tel: +32 43664282; Fax: +32 43662919; Email: jhcaberg{at}student.ulg.ac.be

Human papillomavirus (HPV) infection, particularly type 16, is causally associated with cancer of the uterine cervix. The persistence or progression of cervical lesions suggests that viral antigens are not adequately presented to the immune system. This hypothesis is reinforced by the observation that most squamous intra-epithelial lesions show quantitative and functional alterations of Langerhans cells (LCs). Moreover, E-cadherin-dependent adhesion of LC to keratinocytes (KCs) is defective in cervical HPV16-associated (pre)neoplastic lesions. The possible role of viral oncoprotein E7 in the reduced levels of cell surface E-cadherin was investigated by silencing HPV16 E7 by RNA interference (siRNA). This treatment induced an increased cell surface E-cadherin expression in HPV16-positive KC and a significant adhesion of LC to these squamous cells. The E-cadherin re-expression following HPV16 E7 silencing was associated with increased detection levels of retinoblastoma protein and the activating protein (AP)-2{alpha} transcription factor. These data suggest that HPV16 E7-induced alterations of LC/KC adhesion may play a role in the defective immune response during cervical carcinogenesis.

Abbreviations: AP, activating protein; DC, dendritic cell; HPV, human papillomavirus; IFN, interferon; KC, keratinocyte; LC, Langerhans cell; mRNA, messenger RNA; PCR, polymerase chain reaction; Rb, retinoblastoma; RT, reverse transcription; siC, control siRNA; siE7, E7 siRNA; SIL, squamous intra-epithelial lesion; siRNA, small interfering RNA

{dagger} These authors contributed equally to this work.

Received November 19, 2007; revised June 11, 2008; accepted June 11, 2008.


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