@techreport{oai:kanazawa-u.repo.nii.ac.jp:00052839,
 month = {May},
 note = {すべての肉腫細胞の活性型GSK3βの発現は線維芽細胞より高く, その活性阻害により生存と増殖が抑制され，ミトコンドリア膜電位が低下，消失した. RNA干渉により同様の結果が得られた．これに伴ってmatrix metalloproteinase (MMP)-2の発現が低下し, コラーゲンゲル内での細胞浸潤能が抑制された. マウス移植腫瘍の治療実験では, 対照群（阻害剤の溶媒dimethyl sulfoxide (DMSO) 投与）に比べて，GSK3 β阻害剤投与により腫瘍容積と重量は有意に減少した．また摘出腫瘍では，GSK3 β阻害剤投与群では腫瘍細胞の壊死像を認めた．, Expression of the active form of GSK3β was higher in sarcoma cells than in fibroblasts. Inhibition of GSK3β activity by pharmacological inhibitors or of its expression by RNA interference suppressed the proliferation of sarcoma cells and induced apoptosis. GSK3β inhibition suppressed the expression of cyclin D1, CDK4 and matrix metalloproteinase (MMP)-2 as well as sarcoma cell invasion of collagen gel. Treatment by intraperitoneal injection of either of the GSK3β inhibitors attenuated the proliferation of sarcoma xenografts in mice in comparison to the mice treated with dimethyl sulfoxide (diluent of GSK3β inhibitor). Pathology examination revealed marked necrosis in the tumors of mice treated with the inhibitor. No obvious side effects or adverse events were observed in the treated mice., 研究課題/領域番号:16K20040, 研究期間(年度):2016-04-01 – 2018-03-31, 出典：研究課題「軟部肉腫のGSK3βを標的とする新規治療法の開発と分子メカニズムの解明」課題番号16K20040
（KAKEN：科学研究費助成事業データベース（国立情報学研究所））
（https://kaken.nii.ac.jp/ja/report/KAKENHI-PROJECT-16K20040/16K20040seika/)を加工して作成, 金沢大学附属病院},
 title = {軟部肉腫のGSK3βを標的とする新規治療法の開発と分子メカニズムの解明},
 year = {2018}
}