Scientific article

ADAM15 expression is downregulated in melanoma metastasis compared to primary melanoma

Published inBiochemical and biophysical research communications, vol. 401, no. 3, p. 363-369
Publication date2010

In a mouse melanoma metastasis model it has been recently shown that ADAM15 overexpression in melanoma cells significantly reduced the number of metastatic nodules on the lung. Unfortunately, the expression of ADAM15 in human melanoma tissue has not been determined so far. In our study, we characterized the expression of ADAM15 in tissue micro-arrays of patients with primary melanoma with melanoma metastasis. ADAM15 was expressed in melanocytes and endothelial cells of benign nevi and melanoma tissue. Importantly, ADAM15 was significantly downregulated in melanoma metastasis compared to primary melanoma. We further demonstrate that IFN-gamma and TGF-beta downregulate ADAM15 protein levels in melanoma cells. To investigate the role of ADAM15 in melanoma progression, we overexpressed ADAM15 in melanoma cells. Importantly, overexpression of ADAM15 in melanoma cells reduced the migration, invasion and the anchorage dependent and independent cell growth of melanoma cells. In summary, the downregulation of ADAM15 plays an important role in melanoma progression and ADAM15 act as a tumorsuppressor in melanoma.

  • ADAM Proteins/antagonists & inhibitors/*biosynthesis/genetics
  • Animals
  • Cell Adhesion
  • Cell Line, Tumor
  • Cell Movement
  • Humans
  • Melanoma/enzymology/*pathology
  • Membrane Proteins/antagonists & inhibitors/*biosynthesis/genetics
  • Mice
  • Neoplasm Metastasis
  • Skin Neoplasms/enzymology/*pathology
  • Tumor Suppressor Proteins/antagonists & inhibitors/*biosynthesis/genetics
Affiliation Not a UNIGE publication
Citation (ISO format)
UNGERER, Christopher et al. ADAM15 expression is downregulated in melanoma metastasis compared to primary melanoma. In: Biochemical and biophysical research communications, 2010, vol. 401, n° 3, p. 363–369. doi: 10.1016/j.bbrc.2010.09.055
Main files (1)
ISSN of the journal0006-291X

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