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肿瘤抑制因子miR-34a靶向程序性死亡配体1(PD-L1),并作为急性髓系白血病潜在的免疫治疗靶点发挥作用。

Tumor suppressor miR-34a targets PD-L1 and functions as a potential immunotherapeutic target in acute myeloid leukemia.

作者信息

Wang Xi, Li Jinge, Dong Ke, Lin Fang, Long Min, Ouyang Yongri, Wei Junxia, Chen Xi, Weng Yuanyuan, He Ting, Zhang Huizhong

机构信息

Department of Medical Laboratory and Research Center, Tangdu Hospital, Fourth Military Medical University, Xi'an, PR China.

Department of Medical Laboratory and Research Center, Tangdu Hospital, Fourth Military Medical University, Xi'an, PR China.

出版信息

Cell Signal. 2015 Mar;27(3):443-52. doi: 10.1016/j.cellsig.2014.12.003. Epub 2014 Dec 10.

Abstract

miRNA (miR) 34a has been shown to modulate critical gene transcripts involved in tumorigenesis, but its role in tumor-mediated immunosuppression is largely unknown. PD-L1 plays an important role in immune responses, however, presently its transcriptional regulatory mechanisms are not well understood. In the present study, we analyzed the expression of PD-L1 and miR-34a in 44 acute myeloid leukemia (AML) samples, and observed an inverse correlation between PD-L1 and miR-34a expression. Overexpression of miR-34a in HL-60 and Kasumi-1 cells blocked PD-L1 expression, and reduced PD-L1 surface expression. Using luciferase reporter assay and mutagenesis, we identified miR-34a as a putative binder of the PD-L1-3'UTR. Surface expression of PD-L1 induced by chemotherapeutic agents could also be reversed by miR-34a; furthermore, PD-L1 specific T cell apoptosis was reduced as well following miR-34a transfection. We also found that there is a positive feedback between PD-L1 expression and AKT activation. Our data suggest that miR-34a can regulate PD-L1 expression by targeting PD-L1 mRNA, and our present findings shed new light on the complex regulation of PD-L1 in human tumors, and on miR-34a in cancer immuno-based therapy.

摘要

微小RNA(miR)34a已被证明可调节参与肿瘤发生的关键基因转录本,但其在肿瘤介导的免疫抑制中的作用尚不清楚。程序性死亡配体1(PD-L1)在免疫反应中起重要作用,然而,目前其转录调控机制尚未完全明确。在本研究中,我们分析了44例急性髓系白血病(AML)样本中PD-L1和miR-34a的表达情况,发现PD-L1与miR-34a的表达呈负相关。在HL-60和Kasumi-1细胞中过表达miR-34a可阻断PD-L1的表达,并降低PD-L1的表面表达。通过荧光素酶报告基因检测和诱变,我们确定miR-34a是PD-L1 3'非翻译区(3'UTR)的假定结合物。化疗药物诱导的PD-L1表面表达也可被miR-34a逆转;此外,转染miR-34a后,PD-L1特异性T细胞凋亡也减少。我们还发现PD-L1表达与AKT激活之间存在正反馈。我们的数据表明,miR-34a可通过靶向PD-L1 mRNA来调节PD-L1的表达,我们目前的研究结果为人类肿瘤中PD-L1的复杂调控以及miR-34a在基于癌症免疫治疗中的作用提供了新的线索。

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