let7f‑5p attenuates inflammatory injury in i n vitro pneumonia models by targeting MAPK6

Pneumonia accounts for ~1.3 million mortalities in children per year worldwide. MicroRNAs are implicated in several diseases, including cancer and pneumonia; however, the role of let7f‑5p in pneumonia is not completely understood. In the present study, lipopolysaccharide (LPS) was used to establish an in vitro pneumonia model in A549 and WI‑38 cells. The reverse transcription‑quantitative PCR (RT‑qPCR) and western blotting results demonstrated that let7f‑5p expression levels were significantly decreased, whereas MAPK6 expression levels were significantly increased in the peripheral venous blood of patients with pneumonia and in LPS‑induced A549 and WI‑38 cells compared with healthy volunteers and control cells, respectively. Furthermore, the dual‑luciferase reporter assay demonstrated that let7f‑5p targeted the 3'‑untranslated region of MAPK6. The ELISA and RT‑qPCR results demonstrated that let7f‑5p mimic ameliorated LPS‑induced inflammatory injury in A549 and WI‑38 cells, as demonstrated by decreased expression levels of proinflammatory cytokines, including TNF‑α and IL‑6. In addition, the Cell Counting Kit‑8 assay results indicated that let7f‑5p mimic ameliorated LPS‑induced reductions in cell viability, and the western blotting results demonstrated that let7f‑5p mimic reversed LPS‑induced activation of the STAT3 signaling pathway. Notably, the aforementioned let7f‑5p‑mediated effects were reversed by MAPK6 overexpression. Collectively, the results of the present study suggested that let7f‑5p inhibited inflammation by targeting MAPK6 in the in vitro pneumonia model, thus let7f‑5p may serve as a potential novel therapeutic target for pneumonia.