Objective To study the effects and mechanism of microRNA (miR) -572 on the proliferation and apoptosis of gastric cancer cells. Methods Differences in miR-572 expression between gastric cancer cells and normal gastric mucosal cells was detected by Real-time PCR. NCI-N87 cells transfected with the miR-572 inhibitor were examined using the following techniques: MTT assay of cell proliferation, propidium iodide ( PI) single staining to determine cell cycle distribution, annexin V-fluorescein isothiocyanate / PI to measure apoptosis, and Western blot to detect the expression of cyclin-dependent kinase 4 ( CDK4), p21, B-cell lymphoma / leukemia - 2 ( Bcl-2), and Bcl-2-associated X protein (Bax). An online target gene prediction software identified the gene encoding WW domain-containing oxidoreductase (WWOX) as a possible target of miR-572. This relationship was tested using a luciferase reporter system in which WWOX small interfering RNA ( siRNA) and the miR-572 inhibitor were cotransfected into gastric cancer cells, followed by measurement of cell proliferation, cell cycle distribution and apoptosis as above. Results The expression level of miR-572 in gastric cancer cells was significantly higher than that in normal gastric mucosal cells. Gastric cancer cells transfected with the miR-572 inhibitor showed decreased proliferation, an increased proportion of G1 phase, an increased apoptosis rate, decreased expression of CDK4 and Bcl-2, and increased expression of p21 and Bax protein.,m iR-572 negatively regulated the expression of WWOX protein. WWOX siRNA reversed the inhibitory effect of the miR-572 inhibitor on proliferation, cell cycle arrest and apoptosis of gastric cancer cells. Conclusions Downregulation of miR-572-mediated negative regulation of WWOX inhibited the proliferation of gastric cancer cells, blocked the cell cycle and induced apoptosis.