Compared to adrenocortical adenoma (ACA), adrenocortical carcinoma (ACC) has very poor prognosis and limited treatment options. Also conventional methods to distinguish ACC from ACA can be difficult. At this time, no molecular pathological markers are reliable enough to distinguish either tumor. Recently, increasing data have indicated miRNAs to be crucial regulators in the tumor‑related processes. In the present study, we found that miR-205 expression is significantly suppressed in ACC tissues compared with ACAs, and that this induces apoptosis and impairs proliferation of ACC SW-13 cells in vitro as well as inhibits tumor growth in vivo. Using bioinformatic predictions, Bcl-2 was identified to be a target of miR-205 via 3'-untranslated region (3'UTR) interactions, which was confirmed by luciferase assay, qRT-PCR, immunohistochemical assay and western blotting showing that mRNA and protein expression of Bcl-2 were negatively related to miR-205. Further investigation into the mechanism found that activation of Bcl-2 cleaved Bax, releasing caspase-9 and -3 that are involved in the intrinsic apoptosis pathway, eventually inducing SW-13 cell apoptosis. In conclusion, miR-205 suppresses the growth of ACC SW-13 cells via targeting the anti-apoptotic gene Bcl-2.