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A novel ameloblastoma cell line (AM-3) secretes MMP-9 in response to Wnt-3a and induces osteoclastogenesis

Objective Ameloblastoma has a high risk of bone invasion and local recurrence. However, the mechanisms of bone invasion in ameloblastoma remain unclear. In this study, we established an experimental model for matrix metalloproteinase (MMP) induction and osteoclastogenesis using ameloblastoma-derived...

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Published in:Oral surgery, oral medicine, oral pathology and oral radiology oral medicine, oral pathology and oral radiology, 2013-06, Vol.115 (6), p.780-788
Main Authors: Kibe, Toshiro, DDS, PhD, Fuchigami, Takao, DDS, Kishida, Michiko, PhD, Iijima, Mikio, PhD, Ishihata, Kiyohide, DDS, PhD, Hijioka, Hiroshi, DDS, PhD, Miyawaki, Akihiko, DDS, PhD, Semba, Ichiro, DDS, PhD, Nakamura, Norifumi, DDS, PhD, Kiyono, Tohru, MD, PhD, Kishida, Shosei, MD, PhD
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Language:English
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Summary:Objective Ameloblastoma has a high risk of bone invasion and local recurrence. However, the mechanisms of bone invasion in ameloblastoma remain unclear. In this study, we established an experimental model for matrix metalloproteinase (MMP) induction and osteoclastogenesis using ameloblastoma-derived cells. Study design We established an ameloblastoma-derived cell line without viral genes and analyzed the expression of all Wnt and Frizzled members and MMPs by real-time reverse transcription-polymerase chain reaction, and analyzed the activity of MMP-2 and MMP-9 by the in-gel-gelatinase assay. Results AM-3, newly established ameloblastoma-derived cells retained the morphology of primary-cultured ameloblastoma cells. AM-3 cells overexpressed the messenger RNA of Wnt-5a, Frizzled-2, MMP-2, and MMP-9 and showed the potential of osteoclastogenesis. In addition, Wnt-3a-treatment induced expression and activation of MMP-9 in AM-3 cells. Conclusions Our study suggests that AM-3 cells retained the characteristics of ameloblastoma, without acquiring typical features of cancer cells. Furthermore, Wnt signaling induced MMP-9 in ameloblastoma cells.
ISSN:2212-4403
2212-4411
DOI:10.1016/j.oooo.2013.03.005