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The present study aimed to investigate the potential roles and regulatory mechanism of microRNA (miR)-3941 in lipopolysaccharides (LPS)‑induced acute pneumonia. The expression of miR‑3941 in child patients with acute pneumonia was detected and A549 cells were treated with LPS to establish the cellular model of acute pneumonia. The effects of miR‑3941 in LPS‑induced cell injury were investigated by assessing cell viability, apoptosis and inflammation. In addition, the regulatory relationship between miR‑3941 and insulin‑like growth factor 2 (IGF2) was explored, as well as the association between miR‑3941 and the phosphatidylinositol‑4,5‑bisphosphate 3‑kinase/protein kinase B (PI3K/AKT) pathway. miR‑3941 was significantly down‑regulated in patients with acute pneumonia (P<0.01). In the cell model of acute pneumonia, LPS treatment significantly induced cell injury via inhibiting cell viability (P<0.05 or P<0.01), inducing cell apoptosis (P<0.01) and enhancing the production of cytokines [interleukin (IL)‑6, IL‑8 and tumor necrosis factor‑α; P<0.01 or P<0.001]. LPS treatment also resulted in a significantly decreased expression of miR‑3941 in A549 cells (P<0.01) and the overexpression of miR‑3941 significantly alleviated LPS‑induced cell injury (P<0.05). In addition, IGF2 was confirmed as a direct target gene of miR‑3941. Knockdown of IGF2 significantly alleviated LPS‑induced cell injury (P<0.05, P<0.01 or P<0.001), which was significantly reversed by suppression of miR‑3941 (P<0.05, P<0.01 or P<0.001). Furthermore, inhibition of miR‑3941 was demonstrated to activate the PI3K/AKT pathway, which was inhibited following knockdown of IGF2. The present study indicates that miR‑3941 is downregulated in child patients with acute pneumonia and that downregulation of miR‑3941 may promote LPS‑induced cell injury in A549 cells via targeting IGF2 to regulate the activation of the PI3K/AKT pathway. Therefore, miR‑3941 may be a potential therapeutic target for the treatment of acute pneumonia in child patients.
This article was published in the following journal.
Name: Molecular medicine reports
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