MicroRNA‑217 inhibits the proliferation and invasion, and promotes apoptosis of non‑small cell lung cancer cells by targeting sirtuin 1
- Guangshun Li
- Shouping Zhong
Affiliations: Department of Thoracic, Xi'an Central Hospital, Xi'an, Shaanxi 710003, P.R. China
- Published online on: March 17, 2021 https://doi.org/10.3892/ol.2021.12647
Copyright: © Li
et al. This is an open access article distributed under the
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Non‑small cell lung cancer (NSCLC) is a common malignancy worldwide. MicroRNA (miR)‑217 and sirtuin 1 (SIRT1) have been reported to play significant roles in different types of cancer, such as osteosarcoma and prostate cancer; however, the association between miR‑217 and SIRT1 in the cell proliferation, apoptosis and invasion of NSCLC remain unknown. Thus, the present study aimed to investigate the roles of miR‑217 and SIRT1 in NSCLC. The expression levels of miR‑217 and SIRT1 were detected via reverse transcription‑quantitative (RT‑q)PCR and western blot analyses. The effect of miR‑217 on A549 and H1299 cell proliferation, apoptosis and invasion was assessed via the Cell Counting Kit‑8, flow cytometry and Transwell assays, respectively. In addition, the association between SIRT1 and miR‑217 was predicted using the TargetScan database, and verified via the dual‑luciferase reporter assay, and RT‑qPCR and western blot analyses. The results demonstrated that miR‑217 expression was significantly downregulated, while SIRT1 expression was significantly upregulated in A549 and H1299 cells compared with the human bronchial epithelial cells. Furthermore, transfection with miR‑217 mimic significantly inhibited A549 and H1299 cell proliferation and invasion, and induced A549 and H1299 cell apoptosis. The results of the dual‑luciferase reporter assay and western blot analysis confirmed that SIRT1 is a target gene of miR‑217. In addition, miR‑217 inhibited the activation of AMP‑activated protein kinase (AMPK) and mTOR signaling. Taken together, the results of the present study suggest that miR‑217 inhibits A549 and H1299 cell proliferation and invasion, and induces A549 and H1299 cell apoptosis by targeting SIRT1 and inactivating the SIRT1‑mediated AMPK/mTOR signaling pathway. Thus, miR‑217 may be used as a potential therapeutic target for the treatment of patients with NSCLC.