Dec, 2012
Osteogenic genes related to the canonic WNT pathway are down-regulated in ameloblastoma
Oral Surgery, Oral Medicine, Oral Pathology and Oral Radiology
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- Volume
- 114
- Number
- 6
- First page
- 771
- Last page
- 777
- Language
- English
- Publishing type
- Research paper (scientific journal)
- DOI
- 10.1016/j.oooo.2012.08.453
- Publisher
- ELSEVIER SCIENCE INC
Objective: The aim of this study was to determine the expression of essential osteogenic genes related to the canonic WNT pathway, i.e., WDR5, sFRP-2, and their downstream genes, in ameloblastoma and to clarify their biologic impact on this neoplasm. Study Design: Forty-six paraffin-embedded ameloblastoma samples and ameloblastic (AM-1) and preosteoblastic (KUSA/A1) cell lines were used. Immunohistochemistry, Western blot, reverse-transcription polymerase chain reaction, and alkaline phosphatase (ALP) activity assay were performed. Results: WDR5, essential for osteoblast differentiation and canonic WNT pathway activation, was negative in most ameloblastoma cases and weakly expressed in AM-1 cells. Conversely, sFRP-2s was overexpressed. RUNX2 and C-MYC, downstream inductions of canonic WNT pathway activation, demonstrated weak mRNA expressions in ameloblastoma, suggesting WNT pathway impairment and WDR5 functional inactivity. Recombinant WDR5 weakly induced ALP activity of KUSA/A1 cells cultured in AM-1 conditioned medium. Conclusions: These findings suggest that WNT-related bone-forming genes are down-regulated in ameloblastoma. Concurrent sFRP-2 overexpression suggests that both bone-forming and bone-inhibiting genes equally contributed to reduced bone formation in this neoplasm. © 2012 Elsevier Inc.
- Link information
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- DOI
- https://doi.org/10.1016/j.oooo.2012.08.453
- PubMed
- https://www.ncbi.nlm.nih.gov/pubmed/23159115
- Web of Science
- https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000311370000027&DestApp=WOS_CPL
- Scopus
- https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84869380256&origin=inward
- Scopus Citedby
- https://www.scopus.com/inward/citedby.uri?partnerID=HzOxMe3b&scp=84869380256&origin=inward
- ID information
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- DOI : 10.1016/j.oooo.2012.08.453
- ISSN : 2212-4403
- eISSN : 1528-395X
- Pubmed ID : 23159115
- SCOPUS ID : 84869380256
- Web of Science ID : WOS:000311370000027