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Originally published online as doi:10.2353/ajpath.2008.080136 on October 30, 2008

Published online before print October 30, 2008
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(American Journal of Pathology. 2008;173:1873-1881.)
© 2008 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2008.080136

Semaphorin 3E Expression Correlates Inversely with Plexin D1 During Tumor Progression

Ilse Roodink*, Gürsah Kats*, Léon van Kempen*, Meritha Grunberg*, Cathy Maass*, Kiek Verrijp*, Jos Raats{dagger} and William Leenders*

From the Department of Pathology,* Radboud University Nijmegen Medical Centre, ModiQuest Incorporation and Department of Biomolecular Chemistry,{dagger} Nijmegen Centre for Molecular Life Sciences, Nijmegen, The Netherlands

Plexin D1 (PLXND1) is broadly expressed on tumor vessels and tumor cells in a number of different human tumor types. Little is known, however, about the potential functional contribution of PLXND1 expression to tumor development. Expression of semaphorin 3E (Sema3E), one of the ligands for PLXND1, has previously been correlated with invasive behavior and metastasis, suggesting that the PLXND1-Sema3E interaction may play a role in tumor progression. Here we investigated PLXND1 and Sema3E expression during tumor progression in cases of melanoma. PLXND1 was not expressed by melanocytic cells in either naevi or melanomas in situ, whereas expression increased with invasion level, according to Clark’s criteria. Furthermore, 89% of the metastatic melanomas examined showed membranous PLXND1-staining of tumor cells. Surprisingly, expression of Sema3E was inversely correlated with tumor progression, with no detectable staining in melanoma metastasis. To functionally assess the effects of Sema3E expression on tumor development, we overexpressed Sema3E in a xenograft model of metastatic melanoma. Sema3E expression dramatically decreased metastatic potential. These results show that PLXND1 expression during tumor development is strongly correlated with both invasive behavior and metastasis, but exclude Sema3E as an activating ligand.




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[Abstract] [Full Text] [PDF]


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