{"created":"2023-07-27T06:50:45.696940+00:00","id":43802,"links":{},"metadata":{"_buckets":{"deposit":"2b7062a2-a564-419b-93d3-adc3170a3078"},"_deposit":{"created_by":18,"id":"43802","owners":[18],"pid":{"revision_id":0,"type":"depid","value":"43802"},"status":"published"},"_oai":{"id":"oai:kanazawa-u.repo.nii.ac.jp:00043802","sets":["2812:2813:2817"]},"author_link":["72145","76902"],"item_9_biblio_info_8":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2017-05-26","bibliographicIssueDateType":"Issued"},"bibliographicPageStart":"4p.","bibliographicVolumeNumber":"2015-04-01 – 2017-03-31","bibliographic_titles":[{"bibliographic_title":"平成28(2016)年度 科学研究費補助金 若手研究(B) 研究成果報告書"},{"bibliographic_title":"2016 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":"炎症性ケモカインCCL3を介して腫瘍部位に集積したCCR5発現線維芽細胞が、増殖因子を産生し、大腸がん発症進展過程に重要な役割を果たしていることをこれまでに明らかとしてきた。この結果に基づき、CCR5を標的分子とした大腸がん治療法の可能性を検討した。マウス大腸がん細胞株またはヒト大腸がん細胞株をマウス盲腸壁への同所接種後に、CCR5阻害剤であるマラビロックを投与すると、腫瘍部位への線維芽細胞の集積ならびに線維芽細胞による上皮増殖因子(EGF)の発現の減弱とともに、腫瘍形成が抑制された。以上の結果から、CCL3-CCR5系を標的とした大腸がん治療法の有効性が示唆された。 ","subitem_description_type":"Abstract"},{"subitem_description":"We previously demonstrated that locally-produced CCL3 induce the intra-tumoral accumulation of cancer-associated fibroblast (CAFs), which express CCR5, a specific receptor for CCL3. Based on these observations, we examined the effect of a CCR5 antagonist, maraviroc, on tumor growth arising from intra-cecal injection of either a mouse or a human colon cancer cell line. Oral administration of maraviroc after tumor injection decreased tumor sizes with reductions in numbers of CAFs and epidermal growth factor (EGF) expression by CAFs, but with few effects on leukocyte infiltration. Consistently, CCL3 in vitro induced fibroblasts to migrate and to express EGF, and maraviroc reduced these in vitro effects of CCL3 on fibroblasts. These observations would indicate the potential of maraviroc or other CCR5 inhibitors as a novel therapeutic modality for colon cancer, by targeting the CCL3-CCR5 interaction.","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:15K18406, 研究期間(年度):2015-04-01 – 2017-03-31","subitem_description_type":"Other"},{"subitem_description":"出典：「CCL3-CCR5を介したがん微小環境制御による、がん悪性化進展治療へ向けた研究」研究成果報告書　課題番号15K18406\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-15K18406/15K18406seika/）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":"10.24517/00050144","subitem_identifier_reg_type":"JaLC"}]},"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=50583473"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/search/?qm=50583473","subitem_relation_type_select":"URI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-15K18406/"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-15K18406/","subitem_relation_type_select":"URI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-15K18406/15K18406seika/"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-15K18406/15K18406seika/","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":"2018-06-11"}],"displaytype":"detail","filename":"CA-PR-SASAKI-S-kaken 2017-4p.pdf","filesize":[{"value":"347.3 kB"}],"format":"application/pdf","licensetype":"license_11","mimetype":"application/pdf","url":{"label":"CA-PR-SASAKI-S-kaken 2017-4p.pdf","url":"https://kanazawa-u.repo.nii.ac.jp/record/43802/files/CA-PR-SASAKI-S-kaken 2017-4p.pdf"},"version_id":"45fe1548-abf1-45f9-b4f6-850b221051be"}]},"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":"CCL3-CCR5を介したがん微小環境制御による、がん悪性化進展治療へ向けた研究","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"CCL3-CCR5を介したがん微小環境制御による、がん悪性化進展治療へ向けた研究"},{"subitem_title":"A possible novel anti-cancer treatment targeting CCL3-CCR5 interaction","subitem_title_language":"en"}]},"item_type_id":"9","owner":"18","path":["2817"],"pubdate":{"attribute_name":"公開日","attribute_value":"2018-06-11"},"publish_date":"2018-06-11","publish_status":"0","recid":"43802","relation_version_is_last":true,"title":["CCL3-CCR5を介したがん微小環境制御による、がん悪性化進展治療へ向けた研究"],"weko_creator_id":"18","weko_shared_id":-1},"updated":"2023-07-27T11:34:17.232155+00:00"}