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外体FABP5通过巨细胞脂代谢和免疫微环境重塑驱动HCC的进展

Siyi Luo¹, Rui Tang², Ling Jiang³

¹Department of Pathology, Suining Central Hospital, Suining, Sichuan, China.

Frontiers in immunology

|October 2, 2025

概括

肝细胞癌细胞通过外体释放脂肪酸结合蛋白5 (FABP5),重编程与瘤相关的巨细胞以促进癌症的进展. 准FABP5可能为HCC提供新的治疗策略.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
代谢过程中的代谢.

背景情况:

肝细胞癌 (HCC) 的进展涉及复杂的瘤微环境 (TME) 相互作用.
与瘤相关的巨细胞 (TAMs) 的重编程在HCC中至关重要,但外基因组介导的代谢调节仍然不清楚.

研究的目的:

为了研究HCC细胞如何调节TAM代谢和通过外体细胞的功能.
确定外体脂肪酸结合蛋白5 (FABP5) 在HCC进展和TAM极化中的作用.

主要方法:

从HCC细胞系中分离出外体,并与巨细胞共同培养.
用蛋白质组学,脂质分析,流细胞计和动物模型来评估FABP5的影响.
在体内实验中评估了FABP5在瘤进展中的作用.

主要成果:

由HCC衍生的外基因组将FABP5转移到TAM,重编程它们的脂质代谢并促进M2极化.
外体FABP5激活PPARγ并抑制PPARα信号传递,增加脂质积累和免疫抑制.
高FABP5表达与HCC预后不佳相关;在小鼠模型中,FABP5删除抑制了瘤生长.

结论:

外体FABP5调解HCC和TAM之间的代谢和免疫通信,推动HCC的进展.
FABP5是重塑瘤免疫微环境的关键因素.
FABP5代表了肝细胞癌的潜在治疗标.

关键词:

外基因组是外基因组的组成部分.脂肪酸结合蛋白 5 脂肪酸结合蛋白肝细胞癌是肝细胞癌.脂质新陈代谢脂质新陈代谢与瘤相关的巨细胞.

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