@article{oai:kumadai.repo.nii.ac.jp:00026611,
 author = {末吉, 貴直 and 城野, 博史 and 神力, 悟 and 太田, 和俊 and 太田, 智子 and 田崎, 雅義 and 厚山, 恵理 and 薬師寺, 俊剛 and 植田, 光晴 and 大林, 光念 and 水田, 博志 and 安東, 由喜雄 and Sueyoshi, Takanao and Jono, Hirofumi and Shinriki, Satoru and Ota, Kazutoshi and Ota, Tomoko and Tasaki, Masayoshi and Atsuyama, Eri and Yakushiji, Toshitake and 植田, 光晴 and Ueda, Mitsuharu and Obayashi, Konen and Mizuta, Hiroshi and 安東, 由喜雄 and Ando, Yukio},
 issue = {1},
 journal = {Cancer Letters},
 month = {Mar},
 note = {application/pdf, 論文(Article), Midkine (MK) plays important roles in tumorigenesis, however, the biological function of MK and whether MK can be a therapeutic target in osteosarcoma are unclear.  Here, we found that osteosarcoma tissues showed high MK expression.  MK knockdown by small interfering RNA significantly induced apoptosis in osteosarcoma cells, whereas recombinant MK increased cell proliferation.  Inhibition of MK signaling by anti-MK monoclonal antibody (anti-MK mAb) suppressed growth of osteosarcoma cells both in vitro and in vivo.  Moreover, inhibition of MK function significantly suppressed lung metastasis in xenograft transplantation model.  Targeting MK by anti-MK mAb may have value in the treatment of osteosarcoma., http://www.sciencedirect.com/science/article/pii/S0304383511006306},
 pages = {23--30},
 title = {Therapeutic approaches targeting midkine suppress tumor growth and lung metastasis in osteosarcoma},
 volume = {316},
 year = {2012},
 yomi = {ウエダ, ミツハル and アンドウ, ユキオ}
}