Elucidation of the morphological change and resorption of bone mechanism in the ameloblastoma

2017 Fiscal Year Final Research Report

• Project/Area Number: 26861732
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Surgical dentistry
• Research Institution: Kyushu University
• Principal Investigator: imai yuko 九州大学, 大学病院, 助教 (30592688)
• Project Period (FY): 2014-04-01 – 2018-03-31
• Keywords: ameloblastoma / RANKL / TRP channel

Outline of Final Research Achievements

Mechanisms of proliferation and differentiation in ameloblastoma, an odontogenic tumor, remain unclear. We previously reported that AM-1, a cell line of plexiform ameloblastoma, resorbed peritumoral bone by release of H+ from V-ATPase and Cl- from ClC-7 on its plasma membrane. Moreover, we found that increasing extracellular Ca2+ concentration evoked morphological change and that administration of RANKL facilitated proliferation. Therefore, we aimed to clarify these mechanisms. We performed RT-PCR, Western blot, immunohistochemistry and cell counting using several modulators of RANK receptor signaling cascade and Ca2+ permeable channels. Our results show that TRPV2, V3, V4 and TRPM7 are candidates for Ca2+ influx channels, and that RANKL-induced facilitation of proliferation was caused by upregulation and dephosphorylation of NFATc1 and c2.

Free Research Field

有病者歯科