Affordable Access

Publisher Website

Differential modulation of human beta-defensin-3 expression in human oral epithelial cells by HPV oncoproteins E6 and E7: potential implication in oral cancer

Authors
Journal
Infectious Agents and Cancer
1750-9378
Publisher
Springer (Biomed Central Ltd.)
Publication Date
Volume
7
Identifiers
DOI: 10.1186/1750-9378-7-s1-o11
Keywords
  • Oral Presentation
Disciplines
  • Biology
  • Medicine

Abstract

Differential modulation of human beta-defensin-3 expression in human oral epithelial cells by HPV oncoproteins E6 and E7: potential implication in oral cancer ORAL PRESENTATION Open Access Differential modulation of human beta-defensin-3 expression in human oral epithelial cells by HPV oncoproteins E6 and E7: potential implication in oral cancer Ge Jin1*, Emeka Innocent1, Brian Chow1, Jing Bian1, Jacob Dayan2, Thomas McCormick3, Aaron Weinberg1 From 13th International Conference on Malignancies in AIDS and Other Acquired Immunodeficiencies (ICMAOI) Bethesda, MD, USA. 7-8 November 2011 Background Human papillomaviruses (HPVs) are small, non-enveloped DNA viruses that infect stratified squamous mucosal and cutaneous epithelia, causing diseases ranging from benign warts to invasive tumors. Failure of the immune system to detect and clear persistent HPV infections frequently leads to the development of oral warts and cancer. HPV infec- tion has been etiologically linked with oral warts and a subset of oral squamous cell carcinoma, particularly in HIV infected patients. The incidence of HPV-related oral lesions is increased in HIV+ subjects on highly active anti- retroviral therapy (HAART). We previously showed that tumor cells in oral carcinoma in situ (CIS) lesions overex- press human beta-defensin-3 (hBD-3), an antimicrobial peptide with immunomodulatory capabilities. Expression of hBD-3 in CIS contributes to the local pro-tumor immune response by selectively chemoattracting tumor- associated macrophages and by enhancing tumor develop- ment and progression. Results To elucidate mechanisms by which high-risk HPV could evade immune detection and clearing via infected epithe- lial cells, we investigated if oncoproteins E6 and E7 derived from high-risk HPV-16 modulate the innate immune response of infected epithelial cells and the role of HPV- induced gene expression in orchestrating local immunity. We have found that cancer cells of HPV-related oral and oropharyngeal squamous cell

There are no comments yet on this publication. Be the first to share your thoughts.