Extracellular protease ADAMTS9 suppresses esophageal and nasopharyngeal carcinoma tumor formation by inhibiting angiogenesis

Cancer Res. 2010 Jul 1;70(13):5567-76. doi: 10.1158/0008-5472.CAN-09-4510. Epub 2010 Jun 15.

Abstract

ADAMTS metalloprotease family member ADAMTS9 maps to 3p14.2 and shows significant associations with the aerodigestive tract cancers esophageal squamous cell carcinoma (ESCC) and nasopharyngeal carcinoma (NPC). However, the functional impact of ADAMTS9 on cancer development has not been explored. In this study, we evaluated the hypothesized antiangiogenic and tumor-suppressive functions of ADAMTS9 in ESCC and NPC, in stringent tumorigenicity and Matrigel plug angiogenesis assays. ADAMTS9 activation suppressed tumor formation in nude mice. Conversely, knockdown of ADAMTS9 resulted in clones reverting to the tumorigenic phenotype of parental cells. In vivo angiogenesis assays revealed a reduction in microvessel numbers in gel plugs injected with tumor-suppressive cell transfectants. Similarly, conditioned medium from cell transfectants dramatically reduced the tube-forming capacity of human umbilical vein endothelial cells. These activities were associated with a reduction in expression levels of the proangiogenic factors MMP9 and VEGFA, which were consistently reduced in ADAMTS9 transfectants derived from both cancers. Taken together, our results indicate that ADAMTS9 contributes an important function in the tumor microenvironment that acts to inhibit angiogenesis and tumor growth in both ESCC and NPC.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • ADAM Proteins / biosynthesis*
  • ADAM Proteins / genetics
  • ADAM Proteins / metabolism
  • ADAMTS9 Protein
  • Animals
  • Down-Regulation
  • Endothelial Cells / cytology
  • Enzyme Activation
  • Esophageal Neoplasms / blood supply*
  • Esophageal Neoplasms / enzymology*
  • Esophageal Neoplasms / genetics
  • Female
  • Gene Knockdown Techniques
  • Humans
  • Matrix Metalloproteinase 9 / biosynthesis
  • Matrix Metalloproteinase 9 / genetics
  • Matrix Metalloproteinase 9 / metabolism
  • Mice
  • Mice, Inbred BALB C
  • Mice, Nude
  • Nasopharyngeal Neoplasms / blood supply*
  • Nasopharyngeal Neoplasms / enzymology*
  • Nasopharyngeal Neoplasms / genetics
  • Neovascularization, Pathologic / enzymology
  • Neovascularization, Pathologic / genetics
  • Neovascularization, Pathologic / pathology
  • Transfection
  • Vascular Endothelial Growth Factor A / biosynthesis
  • Vascular Endothelial Growth Factor A / genetics
  • Vascular Endothelial Growth Factor A / metabolism

Substances

  • VEGFA protein, human
  • Vascular Endothelial Growth Factor A
  • ADAM Proteins
  • ADAMTS9 Protein
  • ADAMTS9 protein, human
  • Matrix Metalloproteinase 9