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

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Author: 北嶋, 俊輔ほか

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Publication date: 2015-05-20

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Note (General)：: 金沢大学がん進展制御研究所がん抑制遺伝子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...

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Material Type: 文書・図像類
Title: 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
Author/Editor: 北嶋, 俊輔
Kitajima, Shunsuke
Author Heading: 北嶋, 俊輔
Kitajima, Shunsuke
Publication Date: 2015-05-20
Publication Date (W3CDTF): 2015-05-20
Alternative Title: CCL2 induced by RB inactivation contributes to the formation of tumor-promoting inflammatory microenvironment
Periodical title: 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 = 2014 Fiscal Year Final Research Report
No. or year of volume/issue: 2013-04-01 – 2015-03-31
Volume: 2013-04-01 – 2015-03-31
Pages: 4p.-
Text Language Code: jpn
Subject Heading: RB
CCL2
CCR2
Tumor microenvironment
Target Audience: 一般
Note (General): 金沢大学がん進展制御研究所
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。
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.
研究課題/領域番号:25830077, 研究期間(年度):2013-04-01 – 2015-03-31
DOI: 10.24517/00059567
Access Restrictions: 限定公開
Related Material: https://kaken.nii.ac.jp/ja/search/?kw=90566465
https://kaken.nii.ac.jp/ja/grant/KAKENHI-PROJECT-25830077/
https://kaken.nii.ac.jp/ja/report/KAKENHI-PROJECT-25830077/25830077seika/
Data Provider (Database): 国立情報学研究所 : 学術機関リポジトリデータベース（IRDB）（機関リポジトリ）
https://irdb.nii.ac.jp
Original Data Provider (Database): 金沢大学 : 金沢大学学術情報リポジトリKURA