miR-362 is a recently discovered member of the microRNA family， and it modulates a variety of physical activities and plays an important role in the occurrence and development of many tumors. However， the biological functions of hsa-miR-362-5p in non-small-cell lung carcinoma (NSCLC) are unknown. Transwell assay and colony formation were used to determine the migration， invasion， and proliferation of NSCLC cells . A subcutaneous tumor model in nude mice was established to detect NSCLC tumor growth . The direct binding of miR-362 to the 3'UTR of Semaphorin 3A (Sema3A) was confirmed by luciferase reporter assay. In this study， we found that the level of miR-362 was higher in NSCLC tissues than in adjacent normal tissues and that the level of miR-362 expression was also elevated in five NSCLC cell lines (A549， 95-D， H1299， H292， and H460) relative to a human normal lung epithelial cell line (BEAS2B). Furthermore， miR-362 promoted NSCLC cell invasion， migration， and colony formation and tumor formation . Next， we identified the miR-362 target gene Sema3A， which is significantly correlated with metastasis. Sema3A expression was increased in normal tissues relative to NSCLC tissues. This result is consistent with the fact that miR-362 expression is negatively correlated with Sema3A expression in clinical tissue samples and indicated that miR-362 can regulate Sema3A expression in NSCLC cells and consequently affect NSCLC invasion， migration， and colony formation. Taken together， these findings on the newly identified miR-362/Sema3A axis elucidate the molecular mechanism of NSCLC invasion and migration and could lead to a potential therapeutic target in NSCLC treatment.