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Snail up-regulates proinflammatory mediators and inhibits differentiation in oral keratinocytes

J Guy Lyons1, Vyomesh Patel, Naomi C Roue

  • 1Dermatology Research Laboratories, Central Clinical School, and Key Centre for Microscopy, University of Sydney, New South Wales, Australia. glyons@med.usyd.edu.au

Cancer Research
|June 19, 2008
PubMed

Insights

Snail2 overexpression in head and neck cancers promotes invasion and inflammation. It also impairs keratinocyte differentiation, contributing to early and late stages of malignancy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Snail2, a transcriptional repressor, is overexpressed in head and neck squamous cell carcinomas (HNSCC) and associated with tumor recurrence.
  • Understanding the role of Snail2 in HNSCC pathogenesis is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the mechanisms by which Snail2 contributes to HNSCC development.
  • To elucidate the functional consequences of Snail2 expression in oral keratinocytes.

Main Methods:

  • Cell biological and molecular analyses of oral keratinocytes expressing Snail2.
  • Assays to evaluate monocyte attraction, matrix invasion, cytokine production, and keratinocyte differentiation.
  • Analysis of nuclear factor-kappaB (NF-κB) transcriptional activity and gene expression (ELF3, matriptase-1).

Main Results:

  • Snail2 expression enhanced monocyte attraction and invasion of collagen matrices.
  • Upregulation of proinflammatory cytokines and cyclooxygenase-2 (COX2) was observed.
  • Snail2 impaired keratinocyte desquamation in vitro and repressed ELF3 and matriptase-1 expression.
  • NF-κB activity was only weakly induced by Snail2, insufficient to explain elevated cytokine levels.

Conclusions:

  • Snail2 promotes HNSCC malignancy by enhancing invasion and inflammation.
  • Snail2 impedes keratinocyte terminal differentiation by repressing ELF3 and matriptase-1, contributing to early-stage malignancy.
  • Snail2 plays a role in both early and later stages of HNSCC pathogenesis.

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