Emerging reports have revealed that several microRNAs (miRNAs) are abnormally expressed in non‑small cell lung cancer (NSCLC). miRNAs have been identified as oncogenes or tumor suppressors, and regulate various biological processes including oncogenesis and development. miR‑802 is dysregulated in multiple types of human cancer, and exerts tumor‑suppressive or promoting roles. However, the expression levels and functional roles of miR‑802 in NSCLC remain largely unknown. In the present study, miR‑802 expression was demonstrated to be decreased in NSCLC tissues and cell lines. A low miR‑802 expression was significantly correlated with the tumor stage, lymph node metastasis and brain metastasis in NSCLC patients. Restoring miR‑802 expression inhibited NSCLC cell proliferation and colony formation, induced cell apoptosis, decreased cell migration and invasion in vitro, and hindered in vivo tumor growth. Mechanistically, fibroblast growth factor receptor 1 (FGFR1) was confirmed as the target gene of miR‑802 in NSCLC cells. In addition, FGFR1 silencing mimicked the tumor‑suppressing roles of miR‑802 upregulation in NSCLC cells. Furthermore, rescue experiments revealed that FGFR1 reintroduction rescued the miR‑802‑induced inhibition of the malignant phenotypes in NSCLC cells. Notably, miR‑802 was able to deactivate the phosphoinositide 3‑kinase (PI3K)/AKT serine/threonine kinase (Akt)/mammalian target of rapamycin (mTOR) pathway in NSCLC cells in vitro and in vivo. Overall, these results demonstrated that miR‑802 could downregulate FGFR1 expression, thereby deactivating the PI3K/Akt/mTOR pathway and inhibiting the malignant development of NSCLC. Thus, miR‑802 may be a therapeutic candidate for patients with NSCLC.