The study was done to investigate the effect of LncRNA MEG3 on the immunity and autophagy of non-small cell lung carcinoma through the IDO signaling pathway. A total of 78 cases of early NSCLC patients (research group; RG) and 69 cases of health controls (control group; CG) during the same time were included. The contents of LncRNA MEG3 and miR-543 in peripheral blood and tissues and their diagnostic values for NSCLC were detected. The relationship between LncRNA MEG3 and miR-543 and their posttreatment contents and influence on the prognosis of NSCLC patients were tested. The expression of LncRNA MEG3, miR-543, and IDO (IDO1, IDO2, and TDO proteins) in the lung tissue of rats and the immune function in the CG and the RG were detected. The effects of LncRNA MEG3 and miR-543 on the biological behavior of NSCLC cells were determined. The role of LncRNA MEG3, miR-543, and IDO in NSCLC was verified. LncRNA MEG3 was low in peripheral blood and tissues, while miR-543 was high (P < 0.05); both had good diagnostic values for NSCLC (P < 0.05). LncRNA MEG3 had a negative correlation with miR-543 (P < 0.05) and influenced the prognosis of NSCLC patients (P < 0.05). LncRNA MEG3 in the lung tissue of rats using IDO inhibitor was elevated compared with that of lung carcinoma model rats (P < 0.05). The level of miR-543 was declined compared with that of lung carcinoma model rats (P < 0.05). The levels of IDO1, IDO2, and TDO proteins were evidently declined compared with those of lung carcinoma model rats (P < 0.05). Compared with lung carcinoma model rats, CD3+, CD4+, and CD4+/CD8+ of IDO inhibitor rats were elevated, while CD8+ was declined (P < 0.05). Cell proliferation and invasion ability and IDO1, IDO2, TDO, Beclin-1, and LC3-II proteins were declined in the sh-LncRNA MEG3 group (P < 0.05), while those in the mimics-miR-543 group were evidently elevated (P < 0.05). However, the double luciferase activity detection and RIP experiment confirmed that there was targeted regulation among them (P < 0.05). MEG3 has low expression in NSCLC and affects the immunity and autophagy of NSCLC cells via regulating the miR-543/IDO signaling pathway, which is effective for the treatment of NSCLC.

中文翻译：

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LncRNA MEG3通过IDO信号通路对非小细胞肺癌免疫和自噬的影响

本研究旨在探讨LncRNA MEG3通过IDO信号通路对非小细胞肺癌免疫和自噬的影响。共纳入同期早期NSCLC患者78例（研究组；RG）和健康对照组69例（对照组；CG）。检测外周血和组织中LncRNA MEG3和miR-543的含量及其对NSCLC的诊断价值。检测LncRNA MEG3与miR-543的关系及其治疗后含量及对NSCLC患者预后的影响。检测大鼠肺组织中LncRNA MEG3、miR-543和IDO（IDO1、IDO2和TDO蛋白）的表达以及CG和RG的免疫功能。确定了 LncRNA MEG3 和 miR-543 对 NSCLC 细胞生物学行为的影响。验证了 LncRNA MEG3、miR-543 和 IDO 在 NSCLC 中的作用。LncRNA MEG3在外周血和组织中含量较低，而miR-543含量较高（P < 0.05）；两者均对 NSCLC 具有良好的诊断价值（P < 0.05）。LncRNA MEG3与miR-543呈负相关（P < 0.05），影响NSCLC患者的预后（P < 0.05）。与肺癌模型大鼠相比，使用IDO抑制剂的大鼠肺组织中LncRNA MEG3升高（P < 0.05）。与肺癌模型大鼠相比，miR-543水平下降（P < 0.05）。与肺癌模型大鼠相比，IDO1、IDO2、TDO蛋白水平明显下降（P < 0.05）。与肺癌模型大鼠相比，IDO抑制剂大鼠CD3+、CD4+、CD4+/CD8+升高，CD8+降低（P < 0.05）。sh-LncRNA MEG3组细胞增殖和侵袭能力及IDO1、IDO2、TDO、Beclin-1、LC3-II蛋白均下降（P < 0.05），mimics-miR-543组明显升高（P < 0.05）。 P < 0.05)。但双荧光素酶活性检测和RIP实验证实它们之间存在靶向调控（P < 0.05）。MEG3在NSCLC中低表达，通过调节miR-543/IDO信号通路影响NSCLC细胞的免疫和自噬，对NSCLC的治疗有效。双荧光素酶活性检测和RIP实验证实它们之间存在靶向调控（P < 0.05）。MEG3在NSCLC中低表达，通过调节miR-543/IDO信号通路影响NSCLC细胞的免疫和自噬，对NSCLC的治疗有效。双荧光素酶活性检测和RIP实验证实它们之间存在靶向调控（P < 0.05）。MEG3在NSCLC中低表达，通过调节miR-543/IDO信号通路影响NSCLC细胞的免疫和自噬，对NSCLC的治疗有效。