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.
Background: The study sought to analyze the predictive value of the early measurement of pregnancy associated plasma protein-A (PAPP-A), prealbumin (PAB), C-reactive protein (CRP), brain natriuretic peptide (BNP), and other indicators of heart failure (HF) after acute myocardial infarction (AMI).
Objective. To explore the effect of dapagliflozin on the myocardial fibrosis and the levels of inflammatory factors in heart failure patients. Methods. 60 patients with T2DM who were diagnosed as acute left heart failure or acute exacerbation of chronic left heart failure in the Department of Cardiology of our hospital from November 1, 2020, to December 31, 2021, during hospitalization were the study subjects. According to the treatment regimen, they were divided into the experimental group (EG) which received dapagliflozin and conventional drugs and the control group (CG) which received conventional drugs, with 30 cases in each group to compare and analyze the clinical indicators such as myocardial fibrosis and inflammatory factors. Results. The levels of TNF-α, IL-1β, IL-6, and hs-CRP in the two groups were decreased gradually after treatment, and the levels of TNF-α, IL-1β, IL-6, and hs-CRP in the EG were visibly lower compared with those in the CG at week 4 of treatment (
P
<
0.05
). The cardiac function evaluation of patients showed that the levels of LVEF and LVEDD in both groups were gradually improved after treatment, with a significant difference from the fourth week. In other words, compared with the CG, the LVEF level in the EG was obviously higher (
P
<
0.05
), the LVEDD level was distinctly lower (
P
<
0.05
), and the levels of ST2, BNP, and MCP-1 in the EG were clearly lower at week 4 of treatment (
P
<
0.05
) with a statistical significance in difference. Conclusion. Dapagliflozin has a definite curative effect in heart failure patients with type 2 diabetes mellitus, which can effectively reduce the inflammatory response of patients and inhibit the myocardial fibrosis, and has a potential value in improving cardiac function and promoting prognosis.
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