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Cancer Investigation Volume 29, 2011 - Issue 3
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ORIGINAL ARTICLE: CELLULAR AND MOLECULAR BIOLOGY

Human Beta-Defensin-1, -2, and -3 Exhibit Opposite Effects on Oral Squamous Cell Carcinoma Cell Proliferation

Jochen WinterDepartment of Oral & Maxillofacial Plastic Surgery, Department of Otorhinolaryngology/Surgery, Department of Dermatology and Allergy, Department of Prosthodontics, Preclinical Education and Dental Materials Science, Department of Periodontology, Operative and Preventive Dentistry, University of Bonn, Bonn, Germany
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Annette PantelisDepartment of Oral & Maxillofacial Plastic Surgery, Department of Otorhinolaryngology/Surgery, Department of Dermatology and Allergy, Department of Prosthodontics, Preclinical Education and Dental Materials Science, Department of Periodontology, Operative and Preventive Dentistry, University of Bonn, Bonn, Germany
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Rudolf ReichDepartment of Oral & Maxillofacial Plastic Surgery, Department of Otorhinolaryngology/Surgery, Department of Dermatology and Allergy, Department of Prosthodontics, Preclinical Education and Dental Materials Science, Department of Periodontology, Operative and Preventive Dentistry, University of Bonn, Bonn, Germany
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Markus MartiniDepartment of Oral & Maxillofacial Plastic Surgery, Department of Otorhinolaryngology/Surgery, Department of Dermatology and Allergy, Department of Prosthodontics, Preclinical Education and Dental Materials Science, Department of Periodontology, Operative and Preventive Dentistry, University of Bonn, Bonn, Germany
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Dominik KrausDepartment of Oral & Maxillofacial Plastic Surgery, Department of Otorhinolaryngology/Surgery, Department of Dermatology and Allergy, Department of Prosthodontics, Preclinical Education and Dental Materials Science, Department of Periodontology, Operative and Preventive Dentistry, University of Bonn, Bonn, Germany
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Soeren JepsenDepartment of Oral & Maxillofacial Plastic Surgery, Department of Otorhinolaryngology/Surgery, Department of Dermatology and Allergy, Department of Prosthodontics, Preclinical Education and Dental Materials Science, Department of Periodontology, Operative and Preventive Dentistry, University of Bonn, Bonn, Germany
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Jean-Pierre AllamDepartment of Oral & Maxillofacial Plastic Surgery, Department of Otorhinolaryngology/Surgery, Department of Dermatology and Allergy, Department of Prosthodontics, Preclinical Education and Dental Materials Science, Department of Periodontology, Operative and Preventive Dentistry, University of Bonn, Bonn, Germany
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Natalija NovakDepartment of Oral & Maxillofacial Plastic Surgery, Department of Otorhinolaryngology/Surgery, Department of Dermatology and Allergy, Department of Prosthodontics, Preclinical Education and Dental Materials Science, Department of Periodontology, Operative and Preventive Dentistry, University of Bonn, Bonn, Germany
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Matthias WenghoeferDepartment of Oral & Maxillofacial Plastic Surgery, Department of Otorhinolaryngology/Surgery, Department of Dermatology and Allergy, Department of Prosthodontics, Preclinical Education and Dental Materials Science, Department of Periodontology, Operative and Preventive Dentistry, University of Bonn, Bonn, GermanyCorrespondence[email protected]
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Pages 196-201 | Published online: 31 Jan 2011
 
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Abstract

The objective of this study was to investigate the impact of human beta-defensins (hBDs) on oral squamous cell carcinoma (OSCC) proliferation and hBD expression in vitro. BHY-OSCC cell lines were stimulated with hBD-1, -2, and -3. Proliferation of BHY cells was ascertained and hBD-mRNA expression was evaluated by real-time PCR. Proliferation of BHY cells decreased by 25% in response to hBD-1 stimulation but increased after stimulation with hBD-2 and -3. HBD-1 stimulation enhanced hBD-3 expression, whereas HBD-2 stimulation decreased early hBD-3 expression. HBD-3 stimulation enhanced hBD-1 expression. HBDs profoundly impact on OSCC proliferation and hBD expression in vitro. Therefore, hBD-1 might function as a tumor suppressor gene in OSCCs, while hBD-2 and -3 might be protooncogenes.

ACKNOWLEDGEMENTS

This study was supported by the BONFOR research foundation of the Medical Faculty of the University of Bonn. S. Jepsen, J. P. Allam, N. Novak, and D. Kraus were supported by the Deutsche Forschungsgemeinschaft (KFO 208).

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