{"created":"2023-07-27T06:55:28.199936+00:00","id":51420,"links":{},"metadata":{"_buckets":{"deposit":"637d2dba-52f8-4307-b840-00209719b955"},"_deposit":{"created_by":18,"id":"51420","owners":[18],"pid":{"revision_id":0,"type":"depid","value":"51420"},"status":"published"},"_oai":{"id":"oai:kanazawa-u.repo.nii.ac.jp:00051420","sets":["2812:2813:4014"]},"author_link":["84723","2313"],"item_9_biblio_info_8":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2021-05-25","bibliographicIssueDateType":"Issued"},"bibliographicPageStart":"10p.","bibliographicVolumeNumber":"2019-06-28 - 2121-03-31","bibliographic_titles":[{"bibliographic_title":"令和2(2020)年度 科学研究費補助金 挑戦的研究(萌芽) 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":"TGF-βは上皮細胞の分化誘導により大腸がん発生に対してがん抑制性に作用する。一方で、TGF-βはがん細胞の上皮間葉転換（EMT）誘導により悪性化を誘導する。本研究では、TGF-βファミリーのアクチビンに着目し、ドライバー変異を導入したマウス腸管腫瘍オルガノイドを用いて研究を実施した。アクチビンは良性腫瘍細胞のオルガノイド形成を抑制したが、Kras変異により悪性化形質を獲得したオルガノイドは耐性を示し、さらにp53変異を持つ転移性オルガノイドに対してはEMT様形態変化を誘導した。したがって、Krasとp53変異の蓄積がTGF-βに対する反応スイッチ制御に関わると考えられた。","subitem_description_type":"Abstract"},{"subitem_description":"TGF-β signaling suppresses proliferation of intestinal epithelial cells, while it induces epithelial-mesenchymal transition (EMT) of colon cancer cells. Thus, TGF-β plays either of tumor suppressor or tumor promoter role. However, the underlying mechanism has not been elucidated. In this study, we have examined the role of activin, one of TGF-β family cytokines, using mouse intestinal tumor-derived organoids that carried driver mutations in various combinations. Notably, activin treatment suppressed organoid formation of benign tumor cells, while malignant cells with Kras activation mutation showed resistance to activin-induced cell death. Moreover, metastatic cells with p53 mutation showed EMT-like morphological changes and invasion to collagen gel upon activin stimulation. These results suggest that accumulation of driver mutations in Kras and p53 is a possible switching for responses to TGF-β.","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:19K22558, 研究期間(年度):2019-06-28 - 2121-03-31","subitem_description_type":"Other"},{"subitem_description":"出典：「TGF-betaによる大腸がん抑制作用から悪性化誘導へのスイッチ制御機構の解明」研究成果報告書　課題番号19K22558\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-19K22558/19K22558seika/）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":"10.24517/00057723","subitem_identifier_reg_type":"JaLC"}]},"item_9_publisher_17":{"attribute_name":"公開者","attribute_value_mlt":[{"subitem_publisher":"金沢大学新学術創成研究機構ナノ生命科学研究所"}]},"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=40324610"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/search/?qm=40324610","subitem_relation_type_select":"URI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-19K22558/"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-19K22558/","subitem_relation_type_select":"URI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-19K22558/19K22558seika/"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-19K22558/19K22558seika/","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":"2022-02-03"}],"displaytype":"detail","filename":"CA-PR-OSHIMA-M-kaken 2021-9p.pdf","filesize":[{"value":"145.1 kB"}],"format":"application/pdf","licensetype":"license_11","mimetype":"application/pdf","url":{"label":"CA-PR-OSHIMA-M-kaken 2021-9p.pdf","url":"https://kanazawa-u.repo.nii.ac.jp/record/51420/files/CA-PR-OSHIMA-M-kaken 2021-9p.pdf"},"version_id":"fc4e44a6-bf40-4a76-bcd8-74e347413c34"}]},"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":"TGF-betaによる大腸がん抑制作用から悪性化誘導へのスイッチ制御機構の解明","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"TGF-betaによる大腸がん抑制作用から悪性化誘導へのスイッチ制御機構の解明"},{"subitem_title":"Regulation of colon cancer suppression and malignant progression by TGF-beta signaling","subitem_title_language":"en"}]},"item_type_id":"9","owner":"18","path":["4014"],"pubdate":{"attribute_name":"公開日","attribute_value":"2022-02-03"},"publish_date":"2022-02-03","publish_status":"0","recid":"51420","relation_version_is_last":true,"title":["TGF-betaによる大腸がん抑制作用から悪性化誘導へのスイッチ制御機構の解明"],"weko_creator_id":"18","weko_shared_id":-1},"updated":"2023-07-27T13:53:05.987216+00:00"}