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細胞間シグナル伝達は,単細胞レベルのフェノタイプの移行を強化し,異質な癌細胞集団の堅固な再均衡を促進する
Daniel Lopez1, Darren R Tyson2, Tian Hong3
1Department of Biochemistry & Cellular and Molecular Biology, The University of Tennessee, Knoxville, Knoxville, TN, 37916, USA.
Cell communication and signaling : CCS
|August 28, 2025
まとめ
細胞間通信は癌細胞の可塑性と腫瘍内異質性を促進し,転移と薬剤耐性を促進する. この研究は 信号ネットワークが 癌細胞の様々な状態を 維持する方法を示しています
科学分野:
- 癌 生物学
- コンピュータ生物学
- システム生物学
背景:
- 癌細胞のフェノタイプは,表皮からメゼンキマへの移行 (EMT) のような非遺伝的要因の影響を受け,プラスチックである.
- フェノタイプの可塑性は,腫瘍の異質性,転移,および薬剤耐性を促進する.
- フェノタイプの可塑性,特に細胞間通信のメカニズムは十分に理解されていません.
研究 の 目的:
- 癌細胞のフェノタイプの可塑性における細胞間通信の役割を調査する.
- 信号ネットワークが腫瘍内異質性にどのように影響するか理解する.
- 細胞間相互作用によるEMT関連の遺伝子プログラムとその調節を分析する.
主な方法:
- マルチスケール推論アプローチを用いた単細胞トランスクリプトミックの統合データ分析.
- リガンド-受容体相互作用推論 (CellChat),転写因子活性推定 (decoupleR),および因果信号ネットワーク再構築 (CORNETO) のための計算ツールを使用した.
- 細胞間通信によって形成される人口レベルの動態を研究するために数学モデル (通常の微分方程式) を採用した.
主要な成果:
- 信号相互作用は単細胞のフェノタイプの移行を強化し,小細胞肺がん (SCLC) の腫瘍内異質性を維持する.
- 一般的なシグナリングパターンは,メゼンキマのような癌のサブタイプが,フェノタイプを維持するために他者からのシグナルを使用していることを示しています.
- サブタイプ間のコミュニケーションは,腫瘍集団の異質性を加速し,表型組成を安定させる.
結論:
- 細胞間シグナリングは腫瘍内異質性を決定的に維持する.
- 開発された計算アプローチは,scRNA-seqデータから,細胞間および細胞内シグナリングネットワークを総合的に推論する.
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