| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| 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.
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