Comprehensive analyses of the mechanism of bone destruction by oral cancer

2016 Fiscal Year Final Research Report

• Project/Area Number: 25253098
• Research Category: Grant-in-Aid for Scientific Research (A)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Pathobiological dentistry/Dental radiology
• Research Institution: Tokyo Dental College (2015-2016); Tokyo Medical and Dental University (2013-2014)
• Principal Investigator: Yamaguchi Akira 東京歯科大学, 歯学部, 客員教授 (00142430)
• Co-Investigator(Kenkyū-buntansha): 坂本 啓 東京医科歯科大学, 医歯(薬)学総合研究科, 講師 (00302886) ; 栢森 高 東京医科歯科大学, 医歯(薬)学総合研究科, 助教 (10569841) ; 飯村 忠浩 愛媛大学, プロテオサイエンスセンター, その他 (20282775) ; 樋田 泰浩 北海道大学, 大学病院, 講師 (30399919) ; 間石 奈湖 北海道大学, 遺伝子病制御研究所, 特任助教 (00632423) ; 進藤 正信 北海道大学, 歯学研究科(研究院), 教授 (20162802)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 口腔癌 / 骨破壊 / RANKL / IL-6

Outline of Final Research Achievements

We invested the mechanism underling bone destruction by oral cancer, and obtained the
following results. 1) Fibroblasts locating between cancer cells and bone surface produced IL-6 and its stimulate RANKL synthesis in the fibroblastic cells. 2) Oran cancer cells produced RANKL and it collaborator involved in bone resorption with RANKL synthesized by fibroblasts and osteoblasts. 3) Oral cancer cells produced CXCL2, and it stimulated RANKL production by fibroblastic cells. 4) We succeeded to generate a bone destruction model by transplantation of oral cancer cells into mandibular region of athymic mice.5) Fibroblasts locating between cancer cells and bone surface produced TGF-β and it involved in bone destruction by oral cancers.

Free Research Field

口腔病理学