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向TUG1增强了抗癌免疫力,从而促进了伦瓦提尼布在肝细胞癌中的疗效

Siyao Che¹, Longguang He², Qinshou Chen²

¹Hepatobiliary surgery, Gaozhou People's Hospital, Maoming, Guangdong, China. chesiyao2013@163.com.

Genes and immunity

|September 15, 2025

概括

TUG1通过通过miR-377-3p增加PD-L1表达来促进肝细胞癌 (HCC). 向TUG1可以提高林瓦提尼布在HCC治疗的疗效,提供一种新的治疗策略.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
免疫治疗是一种免疫疗法.

背景情况:

肝细胞癌 (HCC) 是一个重大的全球健康挑战,治疗选择有限.
长非编码RNA TUG1 在HCC病变发生中的作用及其与编程死亡配体1 (PD-L1) 的相互作用仍然不完全理解.

研究的目的:

阐明TUG1在HCC进展中的作用.
研究涉及miR-377-3p和PD-L1.1的TUG1的调节机制.
评估TUG1作为与伦瓦丁尼布 (LEN) 结合的治疗标的潜力.

主要方法:

定量实时PCR (RT-qPCR) 用于基因表达分析.
使用GEO和TCGA数据库进行生物信息分析.
细胞生长和侵入的体外测试 (CCK8,殖民地形成,transwell)
共同培养实验评估CD8+T细胞细胞毒性.
双露西法酶记者测定以确认分子相互作用.
在体内瘤异种移植模型.

主要成果:

在HCC组织中,TUG1显著上调,与晚期和PD-L1表达相关.
伦瓦替尼治疗降低了TUG1和PD-L1水平,增强了抗瘤免疫力.
TUG1的过度表达抵消了伦瓦替尼的疗效,而TUG1的倒置则强化了它.
TUG1作为miR-377-3p的分子海绵,导致PD-L1表达的增加.
结合 TUG1 敲除和 lenvatinib 治疗抑制了 in vivo 的瘤生长.

结论:

TUG1通过菌miR-377-3p来促进HCC的进展和免疫逃避,以调节PD-L1.
通过增强CD8+ T细胞介导的细胞毒性,TUG1 knockdown使HCC对lenvatinib治疗敏感.
TUG1代表了一种有前途的治疗点,用于改善伦瓦替尼在HCC治疗中的疗效.

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