Upregulated expression of long non-coding RNA MEG3 serves as a prognostic biomarker in severe pneumonia children and its regulatory mechanism

Abstract

Severe pneumonia is a high-mortality disorder in children. The expression and underlying effects of lncRNA maternally expressed 3 (MEG3) were detected. The relationships between MEG3 and other parameters were reported by Pearson correlation. The prognostic importance of MEG3 was assessed by Kaplan-Meier (K-M) curve and COX analysis and its diagnostic potential was uncovered by the receiver operating characteristic (ROC) curve. Luciferase activity assay was performed to demonstrate the target gene of MEG3. Elevated expression of MEG3 and reduced microRNA-29 c (miR-29 c) were evaluated in severe pneumonia children, and a negative relationship between MEG3 and miR-29 c was propounded. MEG3 might function as an independent prognostic indicator. The diagnostic efficiency of MEG3 was also indicated for severe pneumonia children. In MRC-5 cell models and MH-S cell models, lipopolysaccharide (LPS) contributed to the increased expression of MEG3. Interference of MEG3 restricted the upregulation of MEG3 triggered by LPS. Silenced MEG3 protected MRC-5 and MH-S cells against damages managed by LPS on cell apoptosis, viability, and inflammation. MiR-29 c was a ceRNA of MEG3 and the absence of MEG3 abrogated the decreased expression of miR-29 c caused by LPS. Overall, the increased expression of MEG3 and the reduced levels of miR-29 c were identified in severe pneumonia. Prognostic and diagnostic significances of MEG3 provided a novel perspective for severe pneumonia. Disruption of MEG3 alleviated cell injury and inflammation as characterized by high LPS by binding miR-29 c.

The long non‐coding RNA maternally expressed 3‐micorRNA‐15a‐5p axis is modulated by melatonin and prevents nucleus pulposus cell inflammation and apoptosis

“…16 Moreover, MEG3 has been demonstrated to be up-regulated in severe pneumonia, and MEG3 knockdown can suppress lipopolysaccharide-elicited MRC-5 and MH-S cell apoptosis and inflammation. 17 Given these outcomes, we speculate that lncRNA MEG3 may also display the function of boosting NP cells' survival and cramping inflammation activation in IVDD.…”

“…By impeding miR‐141 and the AKT (serine/threonine kinase 1)/mTOR (mechanistic target of rapamycin kinase) pathway, lncRNA MEG3 can facilitate cell proliferation and restrain inflammation, hence retarding rheumatoid arthritis progression 16 . Moreover, MEG3 has been demonstrated to be up‐regulated in severe pneumonia, and MEG3 knockdown can suppress lipopolysaccharide‐elicited MRC‐5 and MH‐S cell apoptosis and inflammation 17 . Given these outcomes, we speculate that lncRNA MEG3 may also display the function of boosting NP cells' survival and cramping inflammation activation in IVDD.…”

Long non-coding RNA MEG3 promotes tumor necrosis factor-alpha induced oxidative stress and apoptosis in interstitial cells of cajal via targeting the microRNA-21 /I-kappa-B-kinase beta axis

“…The binding site of miR-21 and MEG3 has been reported in the previous studied [ 32 ], and the binding site of miR-21 and IKKB was predicted by miRwalk ( http://mirwalk.umm.uni-heidelberg.de/ ). Then, Dual-Lumi™ Luciferase Reporter Gene Assay Kit (Beyotime, Shanghai, China) was used to test the binding relationship [ 33 ]. Briefly, the wild type or mutant untranslated region (UTR) of MEG3 or IKKB was cloned to the reporter vector, and then the vector was co-transfected to the HEK cells (Sciencell) with miR-21 mimic or miRNA-NC.…”