Inhibition of invasion and metastasis in oral cancer by targeting urokinase-type plasminogen activator receptor

Oral Oncol. 2005 Nov;41(10):971-7. doi: 10.1016/j.oraloncology.2005.05.013. Epub 2005 Aug 29.

Abstract

There have been reports of strong correlations between poor prognosis in various cancers and concomitant expression of urokinase-type plasminogen activator (uPA) and its surface receptor (uPAR). We and others have previously shown that the uPA system plays a significant role in a subset of head and neck squamous cell carcinoma. In the present study, we found that uPAR is required for invasion and metastasis of highly malignant oral cancer cells (OSC-19). Treating OSC-19 cells with antisense oligonucleotides (AS) targeting uPAR resulted in a dramatic decrease of uPAR mRNA expression. Furthermore, pretreatment with AS or siRNA targeting uPAR inhibited progression of OSC-19 cells in experimental models. These results suggest that overexpression of uPAR increases the invasiveness and metastasis of OSC-19 cells, and that uPAR is a promising therapeutic target for regulation of progression of oral cancer.

MeSH terms

  • Animals
  • Biomarkers, Tumor / metabolism*
  • Carcinoma, Squamous Cell / enzymology*
  • Carcinoma, Squamous Cell / secondary
  • Chick Embryo
  • Humans
  • Mouth Neoplasms / enzymology*
  • Mouth Neoplasms / pathology
  • Neoplasm Invasiveness / prevention & control
  • Receptors, Cell Surface / metabolism*
  • Receptors, Urokinase Plasminogen Activator
  • Reverse Transcriptase Polymerase Chain Reaction
  • Tumor Cells, Cultured
  • Urokinase-Type Plasminogen Activator / antagonists & inhibitors*
  • Urokinase-Type Plasminogen Activator / metabolism

Substances

  • Biomarkers, Tumor
  • PLAUR protein, human
  • Receptors, Cell Surface
  • Receptors, Urokinase Plasminogen Activator
  • Urokinase-Type Plasminogen Activator