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Kitakyūshū, Japan

Jimi E.,2 6 1 Manazuru | Jimi E.,Center for Oral Biological Research | Kokabu S.,2 6 1 Manazuru | Matsubara T.,2 6 1 Manazuru | And 3 more authors.
Oral Science International | Year: 2016

Oral squamous cell carcinoma (OSCC) is the most common malignant tumor in the oral cavity and the head and neck region. Gingival squamous cell carcinomas (SCCs) frequently invade the maxilla or the mandibular bone and are associated with poor prognosis. Recent findings suggest that osteoclasts, rather than OSCC cells, mediate invasion to the bone. Nuclear factor-κB (NF-κB) is constitutively activated in OSCCs and is involved in promoting the invasive characteristics of OSCC. NF-κB activation is also important for receptor activator of NF-κB ligand (RANKL)-induced osteoclastogenesis. NF-κB inhibitors suppress proliferation and stimulate apoptosis of OSCC cells in vitro and in vivo, as well as inhibit matrix metalloproteinase (MMP) production in OSCC. Furthermore, NF-κB inhibitors have been shown to suppress osteoclastogenesis by reducing RANKL expression in animal models. Thus, inhibition of NF-κB activity may constitute a promising therapeutic approach to treat bone-invasive OSCC. In this review, we discuss recent findings, which suggest that bone invasion in OSCC is mediated via NF-κB signaling and may be successfully prevented by NF-κB inhibition. © 2015 Japanese Stomatological Society. Published by Elsevier Ltd.

Yamasaki T.,2 6 1 Manazuru | Yamasaki T.,Kyushu University | Ariyoshi W.,2 6 1 Manazuru | Okinaga T.,2 6 1 Manazuru | And 5 more authors.
Journal of Biological Chemistry | Year: 2014

Background: Dectin 1 is found on myeloid lineage cells and contains an immunoreceptor tyrosine-based activation motif from which signals are associated with bone homeostasis. Results: The dectin 1 agonist curdlan suppresses osteoclastogenesis induced by receptor activator of NF-B ligand (RANKL). Conclusion: Curdlan regulates RANKL-induced osteoclastogenesis. Significance: Curdlan could be a potential therapeutic candidate in treating osteoclast-related diseases. © 2014 by The American Society for Biochemistry and Molecular Biology, Inc.

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