Previous studies have indicated that microRNA (miR)-210-3p is upregulated in NSCLC, however, the specific mechanism underlying the role of miR-210-3p in NSCLC pathogenesis requires further investigation. The aim of the present study was to explore the roles of miR-210-3p in NSCLC and the associated mechanisms. A total of 30 NSCLC tissues and paired adjacent normal tissues were collected for study. Reverse transcription-quantitative polymerase chain reaction was performed to compare the expression of miR-210-3p in the 30 paired cancerous and adjacent normal tissues. Additionally, the expression of miR-210-3p in different NSCLC lines and normal human lung epithelial cell line BEAS-2B were also compared. Furthermore, A549 and H1299 NSCLC cells were cultured and transfected with miR-210-3p inhibitors, and MTT and propidium iodide/annexin V assays were performed to investigate the effects of miR-210-3p inhibition on the proliferation and apoptosis of the cells. RT-qPCR and western blot analyses were also performed to determine the effects of miR-210-3p on the expression levels of SIN3A, B-cell lymphoma 2 (Bcl-2) and Caspase-3. Finally, a reverse experiment was conducted by transfecting A549 cells with miR-210-3p inhibitor and SIN3A small interfering (si)RNA, and a dual-luciferase reporter assay was performed to confirm that SIN3A is a direct target of miR-210-3p. It was observed that miR-210-3p was significantly upregulated in NSCLC tissues compared with the levels in the adjacent normal tissues, and that the expression of miR-210-3p in patients with NSCLC was negatively correlated with the expression of SIN3A in NSCLC tissue. miR-210-3p was also significantly upregulated in different NSCLC cell lines compared with the levels in BEAS-2B cells. The transient downregulation of miR-210-3p in A549 cells led to a significant suppression of cell proliferation and markedly increased cell apoptosis, as well as increased the expression of SIN3A and Caspase-3 and decreased the expression of Bcl-2. On the other hand, co-transfection of miR-210-3p inhibitor and SIN3A siRNA partially blocked miR-210-3p inhibitor-induced pro-apoptotic effects. The results of the dual-luciferase reporter assay demonstrated that SIN3A is a direct target of miR-210-3p. Collectively, these findings indicate that can regulate the proliferation and apoptosis of NSCLC cells by targeting SIN3A. These results suggest that miR-210-3p has the potential to become a novel therapeutic target for the treatment of NSCLC.