Gene expression of oncogenes, antimicrobial peptides, and cytokines in the development of oral leukoplakia

Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2010 Sep;110(3):351-6. doi: 10.1016/j.tripleo.2009.08.013.

Abstract

Objective: The aim of this study was to investigate the expression pattern of oncogenes, antimicrobial peptides, and genes involved in inflammation in leukoplakia of the oral cavity compared with healthy gingiva.

Study design: Biopsies of healthy gingiva (n=20) and leukoplakia (n=20), were obtained during routine surgical procedures. RNA was extracted according to standard protocols. Transcript levels of alpha-defensin (DEFA) 1/3, DEFA-4, S100-A7, deleted-in-oral-cancer (Doc) 1, interleukin (IL) 1beta, IL-6, IL-8, IL-10, tumor necrosis factor (TNF) alpha, cyclooxygenase (Cox) 2, epidermal growth factor (EGF), keratinocyte growth factor (KGF), transforming growth factor (TGF) beta1, TGF-alpha, collagen-IA1 (Col-1), and tenascin-c were analyzed by real-time reverse-transcription polymerase chain reaction. The proteins encoded by the different genes were visualized by immunostaining.

Results: Compared with healthy gingiva (set as 1), there was an increased gene expression of DEFA-4 (179.2-fold), S100-A7 (25.4-fold), EGF (24.8-fold), TGF-beta1 (25.2-fold), and tenascin-c (34.3-fold) in oral leukoplakia. The expression of IL-1beta and Doc-1 was decreased (0.01-fold and 0.2-fold, respectively).

Conclusions: The combination of an increased expression of the antimicrobial peptide DEFA-4, the oncogene S100-A7, EGF, and tenascin-c, and a decreased Doc-1 expression in oral leukoplakia might characterize its potency of malignant transformation. Chronic inflammation seems not to be involved in the development of this lesion.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Case-Control Studies
  • Cell Differentiation / physiology
  • Cell Transformation, Neoplastic / genetics
  • Cell Transformation, Neoplastic / metabolism*
  • Collagen Type I / genetics
  • Collagen Type I / metabolism
  • Collagen Type I, alpha 1 Chain
  • Cyclooxygenase 2 / genetics
  • Cyclooxygenase 2 / metabolism
  • Epidermal Growth Factor / genetics
  • Epidermal Growth Factor / metabolism
  • Fibroblast Growth Factor 7 / genetics
  • Fibroblast Growth Factor 7 / metabolism
  • Gene Expression Profiling*
  • Gingiva / immunology
  • Gingiva / metabolism*
  • Humans
  • Immunohistochemistry
  • Interleukins / genetics
  • Interleukins / metabolism
  • Leukoplakia, Oral / immunology
  • Leukoplakia, Oral / metabolism*
  • RNA / analysis
  • Reference Values
  • S100 Calcium Binding Protein A7
  • S100 Proteins / genetics
  • S100 Proteins / metabolism
  • Tenascin / genetics
  • Tenascin / metabolism
  • Transforming Growth Factor alpha / genetics
  • Transforming Growth Factor alpha / metabolism
  • Transforming Growth Factor beta1 / genetics
  • Transforming Growth Factor beta1 / metabolism
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism
  • Tumor Suppressor Proteins / genetics
  • Tumor Suppressor Proteins / metabolism
  • alpha-Defensins / genetics
  • alpha-Defensins / metabolism

Substances

  • CDK2AP1 protein, human
  • Collagen Type I
  • Collagen Type I, alpha 1 Chain
  • Interleukins
  • S100 Calcium Binding Protein A7
  • S100 Proteins
  • S100A7 protein, human
  • Tenascin
  • Transforming Growth Factor alpha
  • Transforming Growth Factor beta1
  • Tumor Necrosis Factor-alpha
  • Tumor Suppressor Proteins
  • alpha-Defensins
  • Fibroblast Growth Factor 7
  • Epidermal Growth Factor
  • RNA
  • Cyclooxygenase 2