細胞骨格構造による糖解の機械的調節
Jin Suk Park1,2, Christoph J Burckhardt3,4, Rossana Lazcano5
1Lyda Hill Department of Bioinformatics, UT Southwestern Medical Center, Dallas, TX, USA.
Nature
|February 14, 2020
まとめ
細胞はエネルギー代謝を 機械的な環境に適応させます 硬い環境は,フォスフォフルトキナーゼ (PFK) を安定させ,グリコリシスを向上させ,柔らかい環境は,PFKを劣化させ,グリコリシスを減少させます. 癌細胞はPFKを維持することで抵抗します
科学分野:
- 細胞のメカニズムと代謝
- 生化学とがん生物学
背景:
- 細胞微環境のメカニズムは 細胞骨格の再構築を通じて 成長や生存などの細胞機能に影響を与えます
- 細胞のプロセスはエネルギーを消費しますが,メカニカルシグナルへの代謝活動の適応は不明です.
研究 の 目的:
- 細胞が変化するメカニカルシグナルに反応して 代謝活動に適応するかどうかを調べる
- 細胞メカニズムと代謝調節を結びつける分子メカニズムを解明する.
主な方法:
- 異なる硬さの基板でヒト支氣管上皮細胞と非小細胞肺がん細胞を研究した.
- 糖分解の変化,リン酸フルークトキナーゼ (PFK) レベル,トリパートイトモチーフ含有タンパク質21 (TRIM21) とストレス繊維の役割を分析した.
- タンパク質の局所化と細胞骨格の組織を観察するために,プロテアソーム分解検査と顕微鏡を用いた.
主要な成果:
- 細胞を柔らかい基板に移動させると,PFKのプロテアソーム分解によって糖分解を抑制する.
- PFKの分解はTRIM21によって媒介され,その放出はストレス繊維の分解によって引き起こされます.
- 癌細胞はTRIM21をダウンレギュレーションし,硬さ不敏感なストレス繊維にそれを封じ込めることで高糖分解を維持します.
結論:
- 糖分解は,アクトミオシン細胞骨格を通して,細胞の微環境の機械的性質と結合する.
- 正常な細胞は 機械的なシグナルに基づいて エネルギー生産を調整しますが がん細胞は 代謝抵抗性を発揮します
- このメカニズムは 細胞の代謝が組織メカニズムに適応し 癌細胞が代謝調節を回避する方法を示しています
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