MicroRNA‑4485 ameliorates severe influenza pneumonia via inhibition of the STAT3/PI3K/AKT signaling pathway
- Longfei Guo
- Quanhong Wang
- Dongquan Zhang
Affiliations: Department of Critical Care Medicine, Gansu Provincial People's Hospital, Lanzhou, Gansu 730000, P.R. China
- Published online on: September 9, 2020 https://doi.org/10.3892/ol.2020.12078
Copyright: © Guo
et al. This is an open access article distributed under the
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The present study aimed to explore the potential roles and mechanism of microRNA‑4485 (miR‑4485) in severe influenza pneumonia. miR‑4485 expression was detected in patients with severe H1N1 pneumonia using quantitative PCR. Furthermore, the effects of aberrantly expressed miR‑4485 on H1N1‑infected A549 cells were investigated using Cell Counting Kit‑8, terminal deoxynucleotidyl transferase dUTP nick end labeling, western blotting and (ELISA) assays. Furthermore, the regulatory relationships between miR‑4485 and the STAT3‑mediated PI3K/AKT/mTOR signaling pathway were explored using a luciferase reporter and rescue assay. MiR‑4485 expression was downregulated following H1N1 infection and in patients with H1N1 pneumonia. In addition, miR‑4485 alleviated H1N1‑induced A549 cell injury by promoting cell viability and the production of cytokines, as well as reducing apoptosis in A549 cells. Furthermore, STAT3 was revealed to be a target gene of miR‑4485. Additionally, STAT3 silencing reversed the protective effects of miR‑4485 knockdown on H1N1‑induced cell injury via inhibition of the PI3K/AKT/mTOR signaling pathway. In conclusion, miR‑4485 inhibited H1N1‑induced severe pneumonia in A549 cells by targeting STAT3 via the PI3K/AKT/mTOR signaling pathway.