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在AOM/DSS诱导的结直肠瘤发生中LAT1的作用

Yunlong Sui¹, Namiko Hoshi², Norihiro Okamoto³

¹Department of Gastroenterology, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, 510260, China; Division of Gastroenterology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Hyogo, 650-0017, Japan.

Biochemical and biophysical research communications

|February 8, 2025

概括

L型氨基酸载体1 (LAT1) 缺失使结肠炎恶化,但没有影响结肠直肠癌瘤的大小或数量. 炎症可能会在瘤生长中补偿LAT1缺乏.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
胃肠病学胃肠病学

背景情况:

氨基酸载体,如L型氨基酸载体1 (LAT1),对于细胞营养供应至关重要,并与癌症进展有关.
在各种癌症中观察到LAT1过度表达,影响瘤发育,但其在具有慢性炎症背景的结直肠癌 (CRC) 中的具体作用尚不清楚.

研究的目的:

在慢性炎症背景下调查LAT1在结直肠癌发展中的作用.
探索LAT1缺乏对结肠炎相关癌症 (CAC) 进展和瘤微环境的影响.

主要方法:

使用大肠炎相关癌症 (CAC) 鼠标模型,涉及氧甲 (AOM) 和硫酸 (DSS) 治疗.
产生了肠表皮特异性LAT1 (LAT1^fl/fl; vil-cre) 缺失的小鼠,以评估其 in vivo 的功能.
分析了瘤特征,炎症标志物 (IL-1β,IL-6),细胞增殖和细胞亡.

主要成果:

与正常结肠密室相比,LAT1在AOM/DSS诱导的瘤组织中表达高.
在慢性结肠炎阶段,LAT1被删除的小鼠 (LAT1^fl/fl; vil-cre) 显示出更严重的体重减轻.
虽然IL-1β和IL-6的表达在LAT1被删除的瘤中增加,但在LAT1被删除和对照小鼠之间没有观察到结肠瘤数量或大小的显著差异.
细胞增殖和细胞亡率在具有和没有LAT1.1的瘤中相似.

结论:

LAT1 缺乏会加剧慢性结肠炎阶段,并改变结肠直肠瘤内的炎症状态.
在这种CAC模型中,LAT1可能不是整体瘤发展的主要驱动因素,因为炎症可能会补偿氨基酸供应受损.
研究结果表明,针对LAT1的疗法可以用于临床CRC治疗,可能通过调节炎症微环境来探索.

关键词:

在AOM/DSS中使用.结肠直肠癌是一种癌症.炎症炎症是一种炎症.L型氨基酸输送器 1 1

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