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変異したKRASは,ストレス粒子を上昇させ,腫瘍細胞の適性を高めます

Elda Grabocka¹, Dafna Bar-Sagi¹

¹Department of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, NY 10016, USA.

|December 17, 2016

まとめ

ミュータントKRASはストレス粒子の形成を促進し,がん細胞の生存率を高めます. このプロセスは,15-デオキシ-デルタ12,14プロスタグランジンJ2 (15-d-PGJ2) によって駆動され,新しい治療戦略を示唆する保護性腫瘍ニッチを作成します.

科学分野:

腫瘍学
分子生物学
細胞のストレス反応

背景:

腫瘍細胞のストレス対応メカニズムは治療の標的となる可能性があります
ストレス粒子は,ストレス適応に関与する細胞質mRNAとタンパク質の焦点です.

研究の目的:

変異したKRASがん細胞におけるストレス粒子の作用を調査する.
これらの細胞におけるSG形成とストレス抵抗を調節する分子メカニズムを特定する.

主な方法:

ストレス下にある変異したKRAS細胞におけるSGレベルの分析.
SG形成における15-デオキシ-デルタ12,14プロスタグランジンJ2 (15-d-PGJ2) の役割を調査する.
15-d-PGJ2が突然変異した細胞と野生型KRAS細胞の両方のストレス耐性に対する影響を評価する.

主要な成果:

変異したKRAS細胞はストレスでSGレベルが上昇します
SGのアップレギュレーションは15-d-PGJ2の生産に依存しています.
変異したKRAS細胞による15-d-PGJ2の分泌は,隣接する野生型のKRAS細胞のSG形成とストレス抵抗性を高め,耐性腫瘍ニッチを生成する.

結論:

変異したKRASは,15-d-PGJ2とSGの形成を通じて非自律的なストレス抵抗メカニズムを促進します.
このメカニズムは,様々な腫瘍サブクローンを含むストレス耐性ニッチを確立します.
この経路をターゲットにすると腫瘍細胞の集団を根絶する上で重要な役割を果たすかもしれません

キーワード:

KRAS について癌についてプロスタグランディンストレス・グランブル

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