MicroRNA-4485 ameliorates severe influenza pneumonia via inhibition of the STAT3/PI3K/AKT signaling pathway

• Published in: Oncology letters Vol. 20; no. 5; p. 1
• Main Authors: Guo, Longfei, Wang, Quanhong, Zhang, Dongquan
• Format: Journal Article
• Language: English
• Published: Athens D.A. Spandidos 01.11.2020; Spandidos Publications; Spandidos Publications UK Ltd
• Subjects: Age; Apoptosis; Binding sites; Biotechnology; Cytokines; Enzyme-linked immunosorbent assay; H1N1 infection; Health aspects; Infections; Influenza; Luciferase; MicroRNA; microRNA-4485; MicroRNAs; Oncology; PI3K/AKT/mTOR signaling pathway; Pneumonia; Reagents; Scientific equipment industry; severe pneumonia; STAT3; Statistical analysis; Swine flu; Viruses; United States; China
• ISSN: 1792-1074; 1792-1082
• DOI: 10.3892/ol.2020.12078

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.