Effects of LncRNA MEG3 on immunity and autophagy of non-small cell lung carcinoma through IDO signaling pathway

Abstract

Background 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. Methods 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. Results 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). Conclusion 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.

The Role of NcRNAs to Regulate Immune Checkpoints in Cancer

“…LncRNAs are molecular markers of tumor diagnosis and prognosis ( 46 , 121 ). A study showed that the lncRNA MEG3 had a low expression and functioned as a tumor suppresser in NSCLC ( 32 ). In NSCLC cells overexpressing MEG3 , the levels of IDO1, IDO2, TDO, and the autophagy-related Beclin-1 and LC3-II proteins were apparently reduced, whereas that of the autophagy-related LC3-I supermolecule was obviously enhanced ( 122 ).…”

“…In NSCLC cells overexpressing MEG3 , the levels of IDO1, IDO2, TDO, and the autophagy-related Beclin-1 and LC3-II proteins were apparently reduced, whereas that of the autophagy-related LC3-I supermolecule was obviously enhanced ( 122 ). MEG3 regulates the miR-543/IDO signaling pathway to influence the autophagy of lung carcinoma cells ( 32 ). Regulation of the miR-543/IDO signaling pathway by MEG3 can be a treatment option for NSCLC.…”

An integrated analysis of prognostic and immune infiltrates for hub genes as potential survival indicators in patients with lung adenocarcinoma

“…A study on the advanced lung cancer inflammation index, for example, discovered that it can predict shorter overall survival not only in patients with lung adenocarcinoma, but also in patients with other tumors at a low level of expression [ 54 ]. TMED2, MOESIN, DPYSL2, and LncRNA MEG3 have been discovered to enhance the occurrence and development of patients with lung adenocarcinoma via several immune-related regulatory mechanisms [ 55 – 58 ]. Furthermore, the hunt for efficient immune checkpoint inhibitors and indicators to predict the efficacy of immunotherapy is critical.…”

Research progress regarding long-chain non-coding RNA in lung cancer: a narrative review

“…LncRNA MEG3 inhibited cell proliferation, migration, invasion and telomerase activity by downregulating DKC1 ( 67 ). In addition, lncRNA-MEG3 is lowly expressed in NSCLC and affects the immunity and autophagy of NSCLC cells by regulating the miR-543/IDO signaling pathway ( 68 ). The above studies indicate that lncRNA-MEG3 is involved in regulating the occurrence and development of SCLC, and can be used as a potential molecular marker for evaluating the prognosis of SCLC.…”