关键词: PD-1/PD-L1 PFKFB3 lncRNA miR-17-5p tumor immune infiltration

来  源:   DOI:10.2147/OTT.S416155   PDF(Pubmed)

Abstract:
UNASSIGNED: There is growing evidence showing that 6-phosphofructo-2-kinase (PFKFB3) plays crucial roles in different types of human cancers, including LUAD; however, the specific mechanism by which PFKFB3 plays a role in LUAD remains unclear.
UNASSIGNED: We investigated the expression of PFKFB3 and explored the underlying mechanism as well as the correlation with immune markers using several online datasets, such as Tumor Immune Estimate Resource (TIMER), UALCAN, and the Cancer Genome Atlas (TCGA) databases, miRWalk, Targetscan, MiRDB and starBase database. Western blot and immunohistochemistry analysis were performed to verify the corresponding outcomes.
UNASSIGNED: It was shown that the mRNA expression of PFKFB3 was lower in LUAD than in the normal tissues, while its protein expression was not consistent with the mRNA level. The expression of PFKFB3 was correlated with clinicopathological parameters and several signaling pathways. The potential long chain (lnc)RNA/microRNA/PFKFB3 axis and the possible mechanism by which tumor progression in LUAD is promoted was predicted. We obtained the LINC01798/LINC02086/AP000845.1/HAGLR-miR-17-5p-PFKFB3 axis after comprehensive analyses of expression, correlation, and survival. Moreover, the expression of PFKFB3 was positively correlated with immune cells and immune checkpoint expression, including PD-1, PD-L1 and CTLA-4.
UNASSIGNED: The present study demonstrated that noncoding RNAs mediated the upregulation of PFKFB3 and was associated with a poor prognosis and immune tumor infiltration in LUAD.
摘要:
越来越多的证据表明,6-磷酸果糖-2-激酶(PFKFB3)在不同类型的人类癌症中起着至关重要的作用,包括LUAD;然而,PFKFB3在LUAD中发挥作用的具体机制尚不清楚.
我们研究了PFKFB3的表达,并使用几个在线数据集探索了潜在的机制以及与免疫标记的相关性,如肿瘤免疫评估资源(TIMER),UALCAN,和癌症基因组图谱(TCGA)数据库,miRWalk,Targetscan,MiRDB和starBase数据库。进行蛋白质印迹和免疫组织化学分析以验证相应的结果。
结果表明,PFKFB3在LUAD中的mRNA表达低于正常组织,而其蛋白表达与mRNA水平不一致。PFKFB3的表达与临床病理参数和多个信号通路相关。预测了潜在的长链(lnc)RNA/microRNA/PFKFB3轴和促进LUAD中肿瘤进展的可能机制。我们在表达的综合分析后获得了LINC01798/LINC02086/AP000845.1/HAGLR-miR-17-5p-PFKFB3轴,相关性,和生存。此外,PFKFB3的表达与免疫细胞和免疫检查点的表达呈正相关,包括PD-1、PD-L1和CTLA-4。
本研究表明,非编码RNA介导PFKFB3的上调,并与LUAD的不良预后和免疫性肿瘤浸润有关。
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