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Carcinogenesis Advance Access published online on June 19, 2008
Carcinogenesis, 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 Caberg1,*, Pascale Hubert1,*, Dominique Begon1, Michael Herfs1, Patrick Roncarati1, Jacques Boniver1 and Philippe Delvenne1

1 Department of Pathology, GIGA-Cancer, B23, University of Liege, CHU Sart Tilman, 4000 Liege, Belgium

Author to whom correspondence, proofs and reprint requests should be sent: Jean-Hubert Caberg, Department of Pathology B23, CHU Sart Tilman, 4000 LIEGE, BELGIUM, TEL: (32) 43664282, Fax: (32) 43662919, E-mail: 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 intraepithelial lesions (SILs) show quantitative and functional alterations of Langerhans cells (LC). Moreover, E-cadherin-dependent adhesion of LC to keratinocytes (KC) 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 Rb protein and the 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.

Key Words: Human Papillomavirus • Langerhans cells • E-cadherin • RNA interference

* P Hubert and JH Caberg contributed equally to this work

This work was supported by the Belgian Fund for Medical Scientific Research, the CRIV (Centre de Recherche Interuniversitaire en Vaccinologie) with a grant from the Walloon Region and GlaxoSmithKline, the Marshall Programme of the Walloon Region (Neoangio 616476), the L. Fredericq Fund and the Centre Anti-Cancereux près l'Université de Liège. P. Delvenne is a Research Director of the Belgian National Fund for Scientific Research.

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


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