Enhanced expression of podoplanin in ameloblastomas.
OBJECTIVE
Podoplanin, a mucin-type transmembrane glycoprotein, is specifically expressed by lymphatic but not blood vascular endothelial cells, and is also widely expressed in various specialized cell types throughout the body. Recent studies have demonstrated that it mediates a pathway leading to collective cell migration and invasion in vivo and in vitro. In the present study, we carried out an immunohistochemical investigation of podoplanin to clarify whether it is expressed in human ameloblastomas (AMs), which are characterized by locally aggressive behavior with a high rate of recurrence. In addition, we examined the localization of the epithelial marker E-cadherin and the mesenchymal marker vimentin to clarify whether AMs show epithelial-mesenchymal transition (EMT).


METHODS
Paraffin-embedded tissue specimens of 38 AMs were examined immunohistochemically using antibodies against podoplanin, E-cadherin, and vimentin.


RESULTS
Immunohistochemical reactivity for podoplanin was detected in the cell membrane and cytoplasm of most odontogenic tumor epithelial cells in AMs. Podoplanin was expressed strongly in peripheral columnar cells and slightly in central stellate reticulum-like cells. E-cadherin was expressed in central stellate reticulum-like cells and showed decreased expression in peripheral columnar cells. Immunoreactivity for E-cadherin was weak or negative in keratinizing cells of acanthomatous AMs, suggesting terminal differentiation of the tumor cells. Immunohistochemical reactivity for vimentin was found in stromal cells, but partial or no reaction was observed in neoplastic cells.


CONCLUSIONS
Expression of podoplanin in AMs is considered to be associated with neoplastic odontogenic tissues; this molecule might play a role in the collective cell migration of tumor nests in AMs. The pattern of expression of E-cadherin and vimentin suggests that invasion in AMs occurs in the absence of EMT. The migration and invasion mediated by podoplanin in AMs could be related to cytoskeletal reorganization.
González-Alva
Patricia
P
Division of Pathology, Department of Diagnostic and Therapeutic Sciences, Meikai University School of Dentistry, Saitama, Japan. patricia@dent.meikai.ac.jp
Tanaka
Akio
A
Oku
Yuka
Y
Miyazaki
Yuji
Y
Okamoto
Eri
E
Fujinami
Masahiro
M
Yoshida
Noriaki
N
Kikuchi
Kentaro
K
Ide
Fumio
F
Sakashita
Hideaki
H
Kusama
Kaoru
K
D000564:Ameloblastoma / Q000473:pathology*; D015820:Cadherins / Q000032:analysis; D002454:Cell Differentiation; D002462:Cell Membrane / Q000648:ultrastructure; D002465:Cell Movement; D003593:Cytoplasm / Q000648:ultrastructure; D003803:Dentigerous Cyst / Q000473:pathology; D004847:Epithelial Cells / Q000473:pathology; D015972:Gene Expression Regulation, Neoplastic / Q000235:genetics; D006801:Humans; D007365:Intercellular Junctions / Q000473:pathology; D008562:Membrane Glycoproteins / Q000032:analysis*; D009361:Neoplasm Invasiveness; D009364:Neoplasm Recurrence, Local / Q000473:pathology; D017154:Stromal Cells / Q000473:pathology; D014746:Vimentin / Q000032:analysis; D000098853:Podoplanin
D015820:Cadherins; D008562:Membrane Glycoproteins; D014746:Vimentin; C117468:PDPN protein, human; D000098853:Podoplanin