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通过调节PD-L1表达的升级,LncTUG1促进肝细胞癌的免疫逃避

Rongshou Wu¹, Weiwei Liu^1,2, Qingping Yang³

¹Department of Hepatobiliary and Pancreatic Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi, People's Republic of China.

Scientific reports

|October 9, 2023

概括

在肝细胞癌 (HCC) 中,TUG1和PD-L1的高表达与预后不佳相关. 沉默TUG1会减少PD-L1的表达,并通过JAK2/STAT3通路增强抗癌免疫力.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
免疫学免疫学免疫学

背景情况:

肝细胞癌 (HCC) 仍然是全球癌症死亡的主要原因.
尽管有进展,但传统治疗对HCC患者的生存益处有限.
免疫疗法是一个有前途的途径,在各种癌症中具有显著的临床价值.

研究的目的:

调查TUG1在调节PD-L1表达和调解HCC中免疫抑制中的作用.
探索针对TUG1作为HCC治疗策略的潜力.

主要方法:

分析HCC患者数据库,并使用qRT-PCR对HCC组织和细胞系进行验证.
共同培养试验评估TUG1对瘤免疫逃生的影响.
CCK8测试用于评估细胞活力.
西部涂抹和qRT-PCR检查JAK2/STAT3通路调节.

主要成果:

发现TUG1和PD-L1在HCC组织和细胞中显著过度表达.
高表达水平的TUG1和PD-L1与较差的患者预后相关.
抑制TUG1导致PD-L1表达减少,并增强了T细胞介导的癌细胞杀死.
下调TUG1降低了JAK2和STAT3.3的mRNA和蛋白质水平.

结论:

TUG1和PD-L1是HCC的致癌驱动因素,与预后不佳有关.
TUG1通过JAK2 / STAT3信号通路调节PD-L1表达,有助于瘤免疫抑制.
准TUG1是一个潜在的策略,可以克服HCC的免疫逃避.

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