Molecular and Pathologic Analysis of human cementifying fibroma

DOI 34 References
  • Hatano Hiroko
    Department of Oral and Maxillofacial Surgery, Division of Cervico-Gnathostomatology, Graduate School of Biomedical Sciences, Hiroshima University
  • Shigeishi Hideo
    Department of Oral and Maxillofacial Surgery, Division of Cervico-Gnathostomatology, Graduate School of Biomedical Sciences, Hiroshima University
  • Kudo Yasusei
    Department of Oral and Maxillofacial Pathobiology, Graduate School, Division of Frontier Medical Science, Graduate School of Biomedical Sciences, Hiroshima University
  • Higashikawa Koichiro
    Department of Oral and Maxillofacial Surgery, Division of Cervico-Gnathostomatology, Graduate School of Biomedical Sciences, Hiroshima University
  • Tobiume Kei
    Department of Oral and Maxillofacial Surgery, Division of Cervico-Gnathostomatology, Graduate School of Biomedical Sciences, Hiroshima University
  • Takata Takashi
    Department of Oral and Maxillofacial Pathobiology, Graduate School, Division of Frontier Medical Science, Graduate School of Biomedical Sciences, Hiroshima University
  • Kamata Nobuyuki
    Department of Oral and Maxillofacial Surgery, Division of Cervico-Gnathostomatology, Graduate School of Biomedical Sciences, Hiroshima University

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Other Title
  • 骨形成線維腫の病態解明への基礎研究

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Human cementifying fibroma (HCF) is a maxillofacial fibro-osseous lesion, which is composed of fibrous tissue containing varying amounts of mineralized material. However, it is poorly understood because of a significant overlap of clinical, radiological, and histological features of other fibro-osseous lesions, and the process of development consisting of proliferation and differentiation is not clear.<BR>We previously established immortalized cell lines from HCF of the jaw and found that receptor for hyaluronan (HA)-mediated motility (RHAMM) was highly expressed in comparison with normal osteoblasts obtained from normal human mandibular bone by microarray analysis. Interestingly, exogenous HA induced the phosphorylation of CD44 and activated Raf-MEK-ERK signaling. Moreover, RHAMM was able to associate with TPX2 and played a predominant role in the cell cycle in HCF.<BR>We also examined the roles of RHAMM in osteoblastic cells. We generated RHAMM overexpressing MC3T3-E1 cells. In MC3T3-E1 cells, overexpressing RHAMM were located intracellular and activated ERK1/2. The activated ERK1/2 by RHAMM overexpression promoted the cell proliferation and suppressed the osoteogenesis.<BR>Our findings strongly suggest that upregulation of RHAMM is correlated with ossifying fibroma progression and osteogenesis suppression.

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