{"created":"2023-07-27T06:55:24.357006+00:00","id":51239,"links":{},"metadata":{"_buckets":{"deposit":"84a65261-eab9-4723-b097-c445a3d9607f"},"_deposit":{"created_by":18,"id":"51239","owners":[18],"pid":{"revision_id":0,"type":"depid","value":"51239"},"status":"published"},"_oai":{"id":"oai:kanazawa-u.repo.nii.ac.jp:00051239","sets":["2812:2813:4014"]},"author_link":["85788","92668"],"item_9_biblio_info_8":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2021-06-09","bibliographicIssueDateType":"Issued"},"bibliographicPageStart":"5p.","bibliographicVolumeNumber":"2018-04-01 - 2021-03-31","bibliographic_titles":[{"bibliographic_title":"令和2(2020)年度 科学研究費補助金 基盤研究(C) 研究成果報告書"},{"bibliographic_title":"2020 Fiscal Year Final Research Report","bibliographic_titleLang":"en"}]}]},"item_9_creator_33":{"attribute_name":"著者別表示","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{}],"nameIdentifiers":[{},{}]}]},"item_9_description_21":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"分子標的薬の獲得耐性機構として上皮間葉転換(EMT) が注目されており、耐性機構の一因であることが示唆されるが、その克服治療法は確立されていない。オシメルチニブ耐性肺癌細胞を用いた実験では、miR-200cの減少とZEB1の増加によるEMTの誘導が示唆された。100 種類のキナーゼ阻害剤ライブラリを用いた薬物スクリーニングの結果、グリコーゲン合成酵素キナーゼ 3 (GSK-3) 阻害剤が間葉表現型を持つ耐性細胞の増殖を著しく阻害し、アポトーシスを誘導することが示された。これらの結果は、GSK-3阻害がEGFR変異肺癌におけるEMTに起因するオシメルチニブ耐性の克服に有用であることを示唆した。","subitem_description_type":"Abstract"},{"subitem_description":"A novel EGFR tyrosine kinase inhibitor, osimertinib, has marked efficacy in patients with EGFR‐mutant lung cancer. While epithelial‐mesenchymal transition (EMT) plays a role in the resistance to various targeted drugs, its involvement in EGFR inhibitor resistance remains unknown. Preclinical experiments with osimertinib‐resistant lung cancer cells showed that EMT was associated with decreased miR-200c and increased ZEB1 expression. Drug screening from a library of 100 kinase inhibitors indicated that Glycogen synthase kinase‐3 (GSK‐3) inhibitors, such as LY2090314, markedly inhibited the growth and induced apoptosis of resistant cells, specifically those with a mesenchymal phenotype. These results suggest that GSK‐3 inhibition could be useful to circumvent EMT‐associated resistance to osimertinib in EGFR‐mutant lung cancer.","subitem_description_type":"Abstract"}]},"item_9_description_22":{"attribute_name":"内容記述","attribute_value_mlt":[{"subitem_description":"研究課題/領域番号:18K07261, 研究期間(年度):2018-04-01 - 2021-03-31","subitem_description_type":"Other"},{"subitem_description":"出典：「miR-200sを標的とした肺癌のEMTに起因するTKI耐性克服治療の開発」研究成果報告書　課題番号18K07261\n（KAKEN：科学研究費助成事業データベース（国立情報学研究所）） \n（https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-18K07261/18K07261seika/）を加工して作成","subitem_description_type":"Other"}]},"item_9_identifier_registration":{"attribute_name":"ID登録","attribute_value_mlt":[{"subitem_identifier_reg_text":"10.24517/00057542","subitem_identifier_reg_type":"JaLC"}]},"item_9_publisher_17":{"attribute_name":"公開者","attribute_value_mlt":[{"subitem_publisher":"金沢大学がん進展制御研究所"}]},"item_9_relation_28":{"attribute_name":"関連URI","attribute_value_mlt":[{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/search/?qm=10722548"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/search/?qm=10722548","subitem_relation_type_select":"URI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-18K07261/"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-18K07261/","subitem_relation_type_select":"URI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-18K07261/18K07261seika/"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-18K07261/18K07261seika/","subitem_relation_type_select":"URI"}}]},"item_9_version_type_25":{"attribute_name":"著者版フラグ","attribute_value_mlt":[{"subitem_version_resource":"http://purl.org/coar/version/c_ab4af688f83e57aa","subitem_version_type":"AM"}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2022-02-10"}],"displaytype":"detail","filename":"CA-PR-FUKUDA-K-kaken 2021-5p.pdf","filesize":[{"value":"472.8 kB"}],"format":"application/pdf","licensetype":"license_11","mimetype":"application/pdf","url":{"label":"CA-PR-FUKUDA-K-kaken 2021-5p.pdf","url":"https://kanazawa-u.repo.nii.ac.jp/record/51239/files/CA-PR-FUKUDA-K-kaken 2021-5p.pdf"},"version_id":"e321a568-97f8-4095-a23d-4c6c708caa95"}]},"item_language":{"attribute_name":"言語","attribute_value_mlt":[{"subitem_language":"jpn"}]},"item_resource_type":{"attribute_name":"資源タイプ","attribute_value_mlt":[{"resourcetype":"research report","resourceuri":"http://purl.org/coar/resource_type/c_18ws"}]},"item_title":"miR-200sを標的とした肺癌のEMTに起因するTKI耐性克服治療の開発","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"miR-200sを標的とした肺癌のEMTに起因するTKI耐性克服治療の開発"},{"subitem_title":"Development of treatment to overcome TKI resistance caused by EMT in lung cancer","subitem_title_language":"en"}]},"item_type_id":"9","owner":"18","path":["4014"],"pubdate":{"attribute_name":"公開日","attribute_value":"2022-02-10"},"publish_date":"2022-02-10","publish_status":"0","recid":"51239","relation_version_is_last":true,"title":["miR-200sを標的とした肺癌のEMTに起因するTKI耐性克服治療の開発"],"weko_creator_id":"18","weko_shared_id":-1},"updated":"2023-07-27T13:51:45.563012+00:00"}