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miR-122/NEGR1轴通过PI3K/AKT通路和巨细胞调节促进结直肠癌肝脏转移

Shipeng Dai^1,2, Haiwen Zhuang³, Zhuozheng Li⁴

¹Department of General Surgery, Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu Province, China.

Journal of translational medicine

|November 26, 2024

概括

miR-122/NEGR1轴通过增强细胞入侵和M2巨分化促进结直肠癌肝脏转移. 针对这一轴为结直肠癌肝转移提供了潜在的治疗策略.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
生物信息学是一种生物信息学.

背景情况:

大肠直肠癌 (CRC) 是一种常见的胃肠道恶性瘤.
肝转移 (CRLM) 是CRC死亡的主要原因,治疗选择有限.

研究的目的:

确定CRLM的新预测和治疗目标.
研究miR-122/NEGR1轴在CRLM进展中的作用.

主要方法:

生物信息学分析,体外细胞测定 (增殖,入侵,迁移),双露西法酶记者测定,RNA-pulldown.
在体内CRLM小鼠模型,免疫光学,qRT-PCR,ELISA,西部斑点.
对巨细胞极化和信号通路 (PI3K/AKT) 的分析.

主要成果:

在肝转移中,miR-122被上调,NEGR1被下调.
miR-122/NEGR1轴通过PI3K/AKT通路促进了CRC细胞的增殖,入侵和迁移.
减少NEGR1表达促进了M2巨细胞两极分化,加速了肝脏转移.

结论:

miR-122/NEGR1轴是结直肠癌肝脏转移的一个关键驱动因素.
这个轴通过PI3K/AKT信号传递和M2巨细胞极化影响瘤的进展.
miR-122/NEGR1轴代表了CRLM的一个有前途的治疗标.

关键词:

神经元生长调节器 1 1 神经元生长调节器大肠直肠癌肝脏转移的转移.巨细胞的两极分化通过PI3K/AKT路径.据报道,MIR-1222号机器人是一架飞机.

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