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FXRは腸がん幹細胞の増殖を調節する

Ting Fu¹, Sally Coulter², Eiji Yoshihara¹

¹Gene Expression Laboratory, Salk Institute for Biological Studies, La Jolla, CA 92037, USA.

|February 23, 2019

まとめ

高脂肪食とWNTシグナリングの変化は,腸の胆酸 (BAs) を増加させ,Lgr5+幹細胞における大腸がん (CRC) を誘発する. ファルネソイドX受容体 (FXR) の活性化が,CRCの治療策となる可能性があります.

科学分野:

胃腸内科
腫瘍学
分子生物学

背景:

腸内胆酸 (BAs) の増加は,大腸癌 (CRC) のリスクと関連しています.
食事とWNTシグナル伝達経路の変異は,CRCの発症に寄与する.

研究の目的:

ダイエットとWNTシグナル伝達によって変化したBAプロファイルがCRCを促進する方法を調査する.
CRCの進行におけるファルネソイドX受容体 (FXR) の役割と,その治療標的としての可能性を調査する.

主な方法:

高脂肪食とAPC変異の文脈におけるBAプロフィールの分析
Lgr5発現 (Lgr5+) がん幹細胞に対する特定のBAの影響を調査する.
Lgr5+細胞の成長とCRCの進行に対する腸内FXR活性化の影響を評価する.

主要な成果:

APC変異と組み合わせた高脂肪食は,Lgr5+細胞の悪性変異を誘導してBAプロフィールを変化させます.
T-βMCAやDCAのような胆酸はFXRを阻害し,Lgr5+細胞の増殖とDNA損傷を引き起こします.
選択的な腸内FXRの活性化により,Lgr5+細胞の成長が抑制され,CRCの進行が制限されます.

結論:

FXRは腸の自己再生とBAホメオスタシスの調節に重要な役割を果たします.
FXRは,大腸がんの潜在的な治療標的であり,特に食事要因とWNT経路の調節不全を含む場合です.

キーワード:

BA-FXR軸 Lgr5(+) 腸の幹細胞大腸がんの進行遺伝的および食事による危険因子

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