4.4 Article

Fatty-acid-binding protein 5 promotes cell proliferation and invasion in oral squamous cell carcinoma

Journal

JOURNAL OF ORAL PATHOLOGY & MEDICINE
Volume 39, Issue 4, Pages 342-348

Publisher

WILEY
DOI: 10.1111/j.1600-0714.2009.00836.x

Keywords

fatty-acid-binding protein; invasion; matrix metalloproteinases; oral squamous cell carcinoma; proliferation

Funding

  1. National Science Council (Taiwan) [NSC 96-2311-B-006-005-MY3, NSC 97-2314-B-384-003-MY3, NSC 98-3112-B-006-012]
  2. Department of Health (Taiwan) [DOH-TD-B-111-004]
  3. Program to Promote Academic Excellence & Develop World-Class Research Centers (Taiwan)
  4. National Research Program for Genomic Medicine Grants of NSC, Taiwan [NSC 97-3112-B-001-016]

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Background: Oral squamous cell carcinoma (OSCC) is one of the most malignant neoplasms worldwide, and the molecular mechanism of oral tumorigenesis is still unclear. Fatty-acid-binding protein 5 (FABP5) was found in our previous study to be upregulated in oral squamous cell carcinomas by proteomic analysis. The implications of FABP5 overexpression in oral cancer progression have not yet been elucidated. Materials and methods: In this study, the recombinant adeno-associated virus vectors were used to deliver and increase the expression of FABP5 in human OSCC cell lines. U6 promoter-driven short-hairpin RNA (shRNA)-triggered RNA interference was used to block FABP5 gene expression. Transwell Matrigel invasion assay, MTS cell proliferation assay, reverse transcription-polymerase chain reaction, Western blot, and gelatin zymography analysis were used to investigate the effects of FABP5 on cell invasion, growth, and matrix metalloproteinase (MMP) production. Results: Overexpression of FABP5 in oral cancer cells increased cell proliferation and invasiveness by increasing the expression of MMP-9. Silencing FABP5 with shRNA significantly suppressed cell proliferation, MMP-9 activities, and invasiveness. Conclusion: Our study provides the first evidence that FABP5 expression modulated MMP-9 production and the invasive behavior of oral cancer cells and suggests that FABP5 may provide novel targets for therapeutic intervention.

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