{"created":"2023-07-27T06:51:00.481164+00:00","id":44237,"links":{},"metadata":{"_buckets":{"deposit":"25358328-ce91-43ad-9ac9-4a49a489c364"},"_deposit":{"created_by":18,"id":"44237","owners":[18],"pid":{"revision_id":0,"type":"depid","value":"44237"},"status":"published"},"_oai":{"id":"oai:kanazawa-u.repo.nii.ac.jp:00044237","sets":["2812:2813:2818"]},"author_link":["24863","74398"],"item_9_biblio_info_8":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2016-06-09","bibliographicIssueDateType":"Issued"},"bibliographicPageStart":"6p.","bibliographicVolumeNumber":"2014-04-01 - 2016-03-31","bibliographic_titles":[{"bibliographic_title":"平成27(2015)年度 科学研究費補助金 挑戦的萌芽研究 研究成果報告書"},{"bibliographic_title":"2015 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":[{"creatorName":"Takahashi, Chiaki"}],"nameIdentifiers":[{"nameIdentifier":"24863","nameIdentifierScheme":"WEKO"},{"nameIdentifier":"50283619","nameIdentifierScheme":"金沢大学研究者情報","nameIdentifierURI":"http://ridb.kanazawa-u.ac.jp/public/detail.php?kaken=50283619"},{"nameIdentifier":"50283619","nameIdentifierScheme":"研究者番号","nameIdentifierURI":"https://nrid.nii.ac.jp/nrid/1000050283619"}]}]},"item_9_description_21":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"本研究は、RBの非細胞自律的な機能を徹底的に探索することによって、がん微小環境研究に新展開をもたらし、単なるRB研究を超えて、新規かつ汎用性のある制がん標的分子を発見することを目指した。RB不活性化によって誘導されるIL-6-STAT3 サーキットが乳がんの自己複製に寄与することを見出した。RB不活性化によるIL-6の発現誘導には、脂肪酸酸化の亢進によるミトコンドリア活性化とそれによるJNK活性化が寄与することも判明した。また、STAT3の活性化は、ミトコンドリアの呼吸鎖の発現を制御する事によってミトコンドリア由来の活性酸素を抑制し、細胞の自己複製能の維持に関わることも明らかになった。","subitem_description_type":"Abstract"},{"subitem_description":"Retinoblastoma (RB) protein inactivation during tumor progression is often associated with a gain of immature phenotypes and chemo-resistance. Determination of an Rb inactivation signature in the context of gaining undifferentiated phenotype revealed that interleukin (IL)-6 is critically implicated in it. Breast cancers are often characterized by RB pathway inactivation. Low RB expression is linked to poorer prognosis and higher IL-6 expression in cases of breast cancer. IL-6 secreted from human breast cancers appeared to determine their tumor-initiating ability and chemo-resistance by promoting a positive feed forward loop between IL-6 and STAT3. The mechanism whereby RB inactivation increased IL-6 production involved fatty acid oxidation (FAO)-dependent mitochondrial metabolism. In addition, IL-6, via STAT3-mediated feedback to mitochondria, autonomously adjusts mitochondrial superoxide to levels suitable to maintain stem cell-like activity.","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:26640070, 研究期間(年度):2014-04-01 - 2016-03-31","subitem_description_type":"Other"},{"subitem_description":"出典：研究課題「炎症性サーキット―がん悪性進展を促す炎症性微小環境のトリガー」課題番号26640070\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-26640070/26640070seika/）を加工して作成","subitem_description_type":"Other"}]},"item_9_description_5":{"attribute_name":"提供者所属","attribute_value_mlt":[{"subitem_description":"金沢大学がん進展制御研究所","subitem_description_type":"Other"}]},"item_9_identifier_registration":{"attribute_name":"ID登録","attribute_value_mlt":[{"subitem_identifier_reg_text":"10.24517/00050579","subitem_identifier_reg_type":"JaLC"}]},"item_9_relation_28":{"attribute_name":"関連URI","attribute_value_mlt":[{"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/search/?qm=50283619","subitem_relation_type_select":"URI"}},{"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-26640070/","subitem_relation_type_select":"URI"}},{"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-26640070/26640070seika/","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_creator":{"attribute_name":"著者","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"高橋, 智聡"}],"nameIdentifiers":[{"nameIdentifier":"74398","nameIdentifierScheme":"WEKO"},{"nameIdentifier":"50283619","nameIdentifierScheme":"e-Rad","nameIdentifierURI":"https://kaken.nii.ac.jp/ja/search/?qm=50283619"}]}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2018-04-19"}],"displaytype":"detail","filename":"CA-PR-TAKAHASHI-C-kaken 2016-6p.pdf","filesize":[{"value":"234.0 kB"}],"format":"application/pdf","licensetype":"license_11","mimetype":"application/pdf","url":{"label":"CA-PR-TAKAHASHI-C-kaken 2016-6p.pdf","url":"https://kanazawa-u.repo.nii.ac.jp/record/44237/files/CA-PR-TAKAHASHI-C-kaken 2016-6p.pdf"},"version_id":"c72fe7f9-141e-4cb8-8b03-171139d803f0"}]},"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":"炎症性サーキット―がん悪性進展を促す炎症性微小環境のトリガー","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"炎症性サーキット―がん悪性進展を促す炎症性微小環境のトリガー"},{"subitem_title":"Inflammatory circuit that triggers malignant progression","subitem_title_language":"en"}]},"item_type_id":"9","owner":"18","path":["2818"],"pubdate":{"attribute_name":"公開日","attribute_value":"2018-04-20"},"publish_date":"2018-04-20","publish_status":"0","recid":"44237","relation_version_is_last":true,"title":["炎症性サーキット―がん悪性進展を促す炎症性微小環境のトリガー"],"weko_creator_id":"18","weko_shared_id":-1},"updated":"2024-07-01T05:41:20.393661+00:00"}