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在肝细胞癌中,Lnc-CCNH-8通过对PD-L1进行上调来促进免疫逃生

Bixing Zhao^1,2,3, Xiaoyuan Zheng^1,2,3, Yang Wang^1,2

¹The United Innovation of Mengchao Hepatobiliary Technology Key Laboratory of Fujian Province, Mengchao Hepatobiliary Hospital of Fujian Medical University, Fuzhou 350025, P.R. China.

Molecular therapy. Nucleic acids

|February 15, 2024

概括

长非编码RNALnc-CCNH-8通过增加PD-L1表达来促进肝细胞癌免疫逃生. 高水平的外体Lnc-CCNH-8预测HCC患者对免疫检查点抑制剂的反应更好.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
分子生物学分子生物学

背景情况:

肝细胞癌 (HCC) 是一种流行癌症,预后不佳.
免疫检查点抑制剂 (ICI) 对HCC治疗有希望,但反应率较低,缺乏生物标志物.

研究的目的:

研究长非编码RNALnc-CCNH-8在HCC进展中的作用及其作为免疫治疗反应生物标志物的潜力.

主要方法:

评估了HCC组织中的Lnc-CCNH-8表达,并将其与预后相关联.
评估了Lnc-CCNH-8对T细胞和抗瘤免疫的体外和体内影响.
研究了涉及微RNA (miR-217,miR-3173) 和PD-L1调节的分子机制.
在小鼠模型中检查了对抗PD-L1治疗的治疗反应.
在接受ICI治疗的HCK患者中分析了血外体Lnc-CCNH-8水平.

主要成果:

Lnc-CCNH-8在HCC中高度表达,并与预后不佳有关.
升高的Lnc-CCNH-8会损害T细胞功能和抗瘤免疫力.
Lnc-CCNH-8通过海绵miR-217和稳定PD-L1通过miR-3173 / PKP3轴上调节PD-L1.
具有高Lnc-CCNH-8表达的瘤对抗PD-L1疗法的敏感性增加.
高血外体Lnc-CCNH-8水平与HCC患者对ICI的更好的治疗反应相关.

结论:

Lnc-CCNH-8通过一个依赖于miR-217/miR-3173的机制通过调节PD-L1来促进HCC的免疫逃生.
外体Lnc-CCNH-8作为HCC免疫治疗反应的预测生物标志物.

关键词:

在 Lnc-CCNH-8 中.MT:非编码RNAs的使用.在PD-L1中.肝细胞癌是肝细胞癌.免疫系统的逃脱是免疫逃脱.免疫疗法免疫疗法

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