BMC pediatrics · 2026
Clinical significance of LINC01093 in children with severe pneumonia and its regulation of miR‑326/MAPK1 axis.
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Tong Peng, Wang Na
Аннотация
OBJECTIVE: Severe pneumonia (SP) poses a significant threat to the life safety of children. This study aims to investigate the diagnostic and prognostic significance as well as the molecular mechanism of LINC01093 in children with SP.
METHODS: Ninety-eight children with SP and ninety-two healthy children were included in the study. The diagnostic potential of LINC01093 was evaluated using the receiver operating characteristic (ROC) curve. The prognosis and the factors influencing the prognosis were analyzed through the Kaplan-Meier survival curve and the multivariate Cox regression model. An in vitro SP model was constructed by inducing MRC-5 cells with lipopolysaccharide (LPS). The relative expression of genes was measured by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability, apoptosis and levels of inflammatory factors were detected by cell counting kit-8 (CCK-8), flow cytometry and Enzyme-linked immunosorbent assay (ELISA).
RESULTS: Compared with healthy children, LINC01093 and MAPK1 were elevated in the serum of children with SP, while miR-326 was reduced. LINC01093 had a good diagnostic potential between children with SP and healthy children. High LINC01093 expression correlated with poor prognosis. Silencing LINC01093 upregulated the viability of MRC-5 cells induced by LPS, inhibited apoptosis and the levels of inflammatory factors (interleukin-1 beta (IL-1β), IL-6, tumor necrosis factor-alpha (TNF-α)). Inhibiting miR-326 or overexpressing MAPK1 partially reversed the protective effect of LINC01093 silencing on LPS-induced cell damage.
CONCLUSION: Silencing LINC01093 exerts a protective effect against LPS-induced damage by regulating the miR-326/MAPK1 axis. This study provides new experimental evidence for understanding the pathogenesis of SP.
METHODS: Ninety-eight children with SP and ninety-two healthy children were included in the study. The diagnostic potential of LINC01093 was evaluated using the receiver operating characteristic (ROC) curve. The prognosis and the factors influencing the prognosis were analyzed through the Kaplan-Meier survival curve and the multivariate Cox regression model. An in vitro SP model was constructed by inducing MRC-5 cells with lipopolysaccharide (LPS). The relative expression of genes was measured by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability, apoptosis and levels of inflammatory factors were detected by cell counting kit-8 (CCK-8), flow cytometry and Enzyme-linked immunosorbent assay (ELISA).
RESULTS: Compared with healthy children, LINC01093 and MAPK1 were elevated in the serum of children with SP, while miR-326 was reduced. LINC01093 had a good diagnostic potential between children with SP and healthy children. High LINC01093 expression correlated with poor prognosis. Silencing LINC01093 upregulated the viability of MRC-5 cells induced by LPS, inhibited apoptosis and the levels of inflammatory factors (interleukin-1 beta (IL-1β), IL-6, tumor necrosis factor-alpha (TNF-α)). Inhibiting miR-326 or overexpressing MAPK1 partially reversed the protective effect of LINC01093 silencing on LPS-induced cell damage.
CONCLUSION: Silencing LINC01093 exerts a protective effect against LPS-induced damage by regulating the miR-326/MAPK1 axis. This study provides new experimental evidence for understanding the pathogenesis of SP.