Objective：The purpose of this study was to find out the effect and possible mechanism of miR-449c on the occurrence and development of lung adenocarcinoma. Methods：Bioinformatics analysis was used to identify the differentially expressed microRNAs between samples with lung adenocarcinoma patients at high risk of recurrence (disease-free survival ≤6 months) and samples with lung adenocarcinoma patients at low risk of recurrence (disease-free survival >60 months). Target gene prediction and pathway analysis were used to analysis possible mechanisms. RT-PCR was used to detect the expression of miR-449c in lung adenocarcinoma tissues and cell lines. miR-449c and c-Myc were overexpressed in lung adenocarcinoma cell lines by cell transfection experiments. Cell growth activity was determined by CCK-8. Cell cycle and apoptosis were detected by flow cytometry. Western blot analysis was used for relevant protein expression. Results：The results of bioinformatics analysis showed that the expression of miR-449c was significantly decreased in the group of lung adenocarcinoma patients at high risk of recurrence compared with the group of lung adenocarcinoma patients at low risk of recurrence. The expression of miR-449c was significantly correlated with the clinical stage and lymph node metastasis of patients with lung adenocarcinoma. The prognosis of patients with low miR-449c expression was significantly worse than that of patients with high miR-449c expression. Pathway and functional analysis indicated that miR-449c may be involved in cell cycle progression. Compared with normal tissues, miR-449c was significantly lower expressed in lung adenocarcinoma tissues. Overexpression of miR-449c inhibited lung adenocarcinoma cell proliferation, resulted in cell cycle arrest in G1 phase, and downregulated the expression of c-Myc and its downstream cyclins. Overexpression of c-Myc could counteract the inhibition of cyclin by miR-449c. Overexpression of miR-449c could also counteract the up-regulation of cyclin expression by c-Myc. Conclusion：Lung adenocarcinoma patients with low expression of miR-449c had a poor prognosis. Overexpression of miR-449c could regulate the lung adenocarcinoma cell cycle by downregulating c-Myc and inhibited the proliferation of lung adenocarcinoma cells. The results suggested that miR-449c may be one of the potential therapeutic targets for lung adenocarcinoma.