ストレス誘発細胞老化は炎症・がん細胞増殖促進に関与する

細胞老化は細胞増殖を停止させることで,がん抑制機構として長らく考えられてきた.しかしながら近年では,細胞老化はがん抑制の他に,発生,組織の老化,損傷修復など,様々な機能があることがわかってきた.驚くべきことに,p53変異,欠失などのある一定の条件下では,細胞老化は分泌因子を介してがん促進に寄与することもわかってきた.老化細胞は炎症性サイトカイン,ケモカイン,増殖因子,マトリックスリモデリング因子などの分泌(senescence-associated secretory phenotype; SASP)を亢進させ,周辺環境を変化させる.そのようなSASP因子は,細胞老化が多面的機能を持つ要因とな...

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Published inThermal Medicine Vol. 35; no. 4; pp. 41 - 58
Main Authors 小橋川, 新子, 坂口, 義彦, 増永, 慎一郎, 森, 英一朗
Format Journal Article
LanguageEnglish
Published 日本ハイパーサーミア学会 15.12.2019
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ISSN1882-2576
1882-3750
DOI10.3191/thermalmed.35.41

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Abstract 細胞老化は細胞増殖を停止させることで,がん抑制機構として長らく考えられてきた.しかしながら近年では,細胞老化はがん抑制の他に,発生,組織の老化,損傷修復など,様々な機能があることがわかってきた.驚くべきことに,p53変異,欠失などのある一定の条件下では,細胞老化は分泌因子を介してがん促進に寄与することもわかってきた.老化細胞は炎症性サイトカイン,ケモカイン,増殖因子,マトリックスリモデリング因子などの分泌(senescence-associated secretory phenotype; SASP)を亢進させ,周辺環境を変化させる.そのようなSASP因子は,細胞老化が多面的機能を持つ要因となっている.本総説では,慢性炎症,がん促進に着目した,細胞老化に関する分子,細胞レベルで得られている知見を紹介する.
AbstractList 細胞老化は細胞増殖を停止させることで,がん抑制機構として長らく考えられてきた.しかしながら近年では,細胞老化はがん抑制の他に,発生,組織の老化,損傷修復など,様々な機能があることがわかってきた.驚くべきことに,p53変異,欠失などのある一定の条件下では,細胞老化は分泌因子を介してがん促進に寄与することもわかってきた.老化細胞は炎症性サイトカイン,ケモカイン,増殖因子,マトリックスリモデリング因子などの分泌(senescence-associated secretory phenotype; SASP)を亢進させ,周辺環境を変化させる.そのようなSASP因子は,細胞老化が多面的機能を持つ要因となっている.本総説では,慢性炎症,がん促進に着目した,細胞老化に関する分子,細胞レベルで得られている知見を紹介する.
Author 増永, 慎一郎
坂口, 義彦
小橋川, 新子
森, 英一朗
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  fullname: 坂口, 義彦
  organization: 奈良県立医科大学,医学部,未来基礎医学
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  fullname: 増永, 慎一郎
  organization: 京都大学複合原子力科学研究所,放射線生命科学研究部門,粒子線生物学研究分野
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  fullname: 森, 英一朗
  organization: 奈良県立医科大学,医学部,未来基礎医学
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Snippet 細胞老化は細胞増殖を停止させることで,がん抑制機構として長らく考えられてきた.しかしながら近年では,細胞老化はがん抑制の他に,発生,組織の老化,損傷修復など,...
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Title ストレス誘発細胞老化は炎症・がん細胞増殖促進に関与する
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