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ID 112332
著者
Ando, Toshinori Hiroshima University
工藤, 保誠 Hiroshima University|The University of Tokushima 徳島大学 教育研究者総覧 KAKEN研究者をさがす
Iizuka, Shinji Hiroshima University
常松, 貴明 Hiroshima University|The University of Tokushima 徳島大学 教育研究者総覧 KAKEN研究者をさがす
Umehara, Hanako Hiroshima University
Shrestha, Madhu Hiroshima University
Matsuo, Toshihiro Aichi Medical University
Kubo, Tadahiko Hiroshima University
Shimose, Shouji Kure Medical Center
Arihiro, Koji Hiroshima University
Ogawa, Ikuko Hiroshima University
Ochi, Mitsuo Hiroshima University
Takata, Takashi Hiroshima University
資料タイプ
学術雑誌論文
抄録
Ameloblastin (AMBN), the most abundant non-amelogenin enamel matrix protein, plays a role in ameloblast differentiation. Previously, we found that AMBN promoted osteogenic differentiation via the interaction between CD63 and integrin β1, leading to the inactivation of Src; however, how AMBN affects the malignant behavior of osteosarcoma is still unclear. Osteosarcoma affects the bone and is associated with poor prognosis because of the high rate of pulmonary metastases and drug resistance. Here we demonstrated that stable overexpression of AMBN induced apoptosis and suppressed colony formation and cell migration via the inactivation of Src-Stat3 pathway in human osteosarcoma cells. Moreover, AMBN induced chemosensitivity to doxorubicin. Thus, AMBN induced a tumor suppressive phenotype and chemosensitivity to doxorubicin via the AMBN-Src-Stat3 axis in osteosarcoma. Indeed, immunohistochemical expression of AMBN was significantly correlated with better outcome of osteosarcoma patients. Our findings suggest that AMBN can be a new prognostic marker and therapeutic target for osteosarcoma combined with conventional doxorubicin treatment.
掲載誌名
Scientific Reports
ISSN
20452322
出版者
Springer Nature
7
開始ページ
40187
発行日
2017-01-05
備考
Supplementary Information : srep_7_40187_s1.pdf
権利情報
© The Author(s) 2017
This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
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出版社版DOI
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言語
eng
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出版社版
部局
歯学系
医学系