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Rbによるサイトカインを介したがん悪性化制御機構の解明
https://doi.org/10.24517/00059567
https://doi.org/10.24517/00059567776dad7a-de8b-4b56-a70b-a2f39b5e3ee1
名前 / ファイル | ライセンス | アクション |
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CA-PR-KITAJIMA-S-kaken 2015-4p.pdf (412.8 kB)
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Item type | 報告書 / Research Paper(1) | |||||
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公開日 | 2020-10-08 | |||||
タイトル | ||||||
タイトル | Rbによるサイトカインを介したがん悪性化制御機構の解明 | |||||
タイトル | ||||||
言語 | en | |||||
タイトル | CCL2 induced by RB inactivation contributes to the formation of tumor-promoting inflammatory microenvironment | |||||
言語 | ||||||
言語 | jpn | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_18ws | |||||
資源タイプ | research report | |||||
ID登録 | ||||||
ID登録 | 10.24517/00059567 | |||||
ID登録タイプ | JaLC | |||||
著者別表示 |
Kitajima, Shunsuke
× Kitajima, Shunsuke |
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提供者所属 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 金沢大学がん進展制御研究所 | |||||
書誌情報 |
平成26(2014)年度 科学研究費補助金 若手研究(B) 研究成果報告書 en : 2014 Fiscal Year Final Research Report 巻 2013-04-01 – 2015-03-31, p. 4p., 発行日 2015-05-20 |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | がん抑制遺伝子RBの不活性化は、がんの悪性進展過程において頻繁に観察される。私達はこれまでに、特定のがん細胞において、RBの追加的不活性化によりサイトカイン分泌亢進依存的にがん幹細胞様性質が誘導されることを明らかにした。本研究では、特にCCL2の発現亢進に着目し、その分子機構として、RB不活性化に伴う酸化ストレス増大、それに続くJNK活性化が関与することを明らかにした。さらに、CCR2(CCL2受容体)欠損マウスへの腫瘍移植実験およびRB欠損依存的乳がんマウスモデルの解析を行い、RB不活性化によるCCL2発現亢進が、特にGr-1陽性血球細胞のがん微小環境中への遊走に寄与することを明らかにした。 | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Inactivation of RB gene is frequently found during tumor progression and correlated with drug resistance or undifferentiated state in some kinds of cancer. We previously found that RB inactivation contributes to the acquisition of stem cell-like activity via activation of inflammatory signaling. But the receptors of some cytokines induced by RB inactivation such as CCL2 were not expressed in tumor cells themselves. Up-regulation of CCL2 secretion was dependent on ROS accumulation and subsequent JNK activation caused by RB inactivation. RB inactivated myofibrosarcoma cells highly expressed CCL2. And these cells showed higher tumorigenic activity in wild type mice but not in CCR2 knockout mice. Angiogenesis and infiltration of Gr-1 positive cells into tumor microenvironment were decreased in CCR2 knockout mice compared with wild type mice. Here we state that CCL2 induced by RB inactivation contributes to the formation of tumor-promoting inflammatory microenvironment. | |||||
内容記述 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 研究課題/領域番号:25830077, 研究期間(年度):2013-04-01 – 2015-03-31 | |||||
内容記述 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 出典:研究課題「Rbによるサイトカインを介したがん悪性化制御機構の解明」課題番号25830077 (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-25830077/25830077seika/)を加工して作成 |
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著者版フラグ | ||||||
出版タイプ | AM | |||||
出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||
関連URI | ||||||
識別子タイプ | URI | |||||
関連識別子 | https://kaken.nii.ac.jp/ja/search/?kw=90566465 | |||||
関連名称 | https://kaken.nii.ac.jp/ja/search/?kw=90566465 | |||||
関連URI | ||||||
識別子タイプ | URI | |||||
関連識別子 | https://kaken.nii.ac.jp/ja/grant/KAKENHI-PROJECT-25830077/ | |||||
関連名称 | https://kaken.nii.ac.jp/ja/grant/KAKENHI-PROJECT-25830077/ | |||||
関連URI | ||||||
識別子タイプ | URI | |||||
関連識別子 | https://kaken.nii.ac.jp/ja/report/KAKENHI-PROJECT-25830077/25830077seika/ | |||||
関連名称 | https://kaken.nii.ac.jp/ja/report/KAKENHI-PROJECT-25830077/25830077seika/ |