c-MycがmiR-23a/bを抑制すると,ミトコンドリアのグルタミンゼ発現とグルタミンミン代謝が強化されます
Ping Gao1, Irina Tchernyshyov, Tsung-Cheng Chang
1Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. pgao2@jhmi.edu
Nature
|February 17, 2009
まとめ
腫瘍性転写因子c-Myc (Myc) は,マイクロRNAを抑制し,ガン細胞におけるグルタミンゼ発現とグルタミンリン代謝を増加させる. これは,Myc,microRNAs,およびがん細胞のエネルギー調節の間の新しいリンクを明らかにします.
科学分野:
- 腫瘍学 腫瘍学
- 分子生物学は分子生物学である.
- バイオケミストリー バイオケミストリー
背景:
- 癌細胞は,ウォーバーグ効果やグルタミノリシスへの依存など,代謝の変化を示します.
- グルタミンは,がん細胞のエネルギー,生物合成,増殖に不可欠ですが,代謝の調節は不明です.
研究 の 目的:
- グルタミン代謝の調節におけるc-Myc腫瘍性転写因子の役割を調査する.
- c-MycとマイクロRNAの調節と癌細胞の代謝を結びつける分子メカニズムを解明する.
主な方法:
- miR-23aとmiR-23bのc-Mycによる転写調節に関する分析.
- ヒトリンパ腫および前立腺がん細胞系におけるグルタミン酶発現およびグルタミン分解の評価 (P-493 BおよびPC3).
主要な成果:
- c-Mycは,miR-23aとmiR-23bを転写的に抑制する.
- この抑制は,ミトコンドリアのグルタミナーゼの発現が増加し,グルタミンの分解性を高めます.
- 上調されたグルタミン代謝はATPの生成とグルタチオンの合成をサポートします.
結論:
- c-Mycは,マイクロRNA抑制を通じてグルタミンゼ発現を調節し,がん細胞の代謝に影響を与えます.
- この研究は,c-Myc,microRNA,グルタミン代謝,および細胞エネルギーホメオスタシスの間の新しい関連性を明らかにしています.
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