Previous studies have demonstrated that microRNA (miR)-205-5p expression is significantly increased in non­small cell lung cancer tissues and is associated with tumor differentiation grade. The aim of the present study was to explore the effects of miR­205­5p on viability, apoptosis and invasion of lung cancer A549 cells. The hsa­miR­205­5p small interfering RNA (siRNA) inhibitor was transfected into A549 cells and expression of miR­205­5p was detected by reverse transcription­quantitative polymerase chain reaction (RT­qPCR). Cell viability, apoptosis and invasion were assayed by Cell Counting kit­8, Annexin V/propidium iodide double staining and Transwell assay, respectively. Target genes of miR­205­5p were predicted using bioinformatics analysis. Expression of mRNA and protein levels of candidate target genes following miR­205­5p inhibition were detected using RT­qPCR and western blot analysis respectively. The results demonstrated that relative survival rates of A549 cells were significantly inhibited in miR­205­5p siRNA­transfected cells at 24 and 48 h compared with control cells. Apoptosis was markedly increased in the miR­205­5p siRNA cells compared with control cells. The number of invaded cells following miR­205­5p siRNA silencing was significantly decreased compared with control cells. Bioinformatics analysis revealed that erb­B2 receptor kinase 3 (erbB3), zinc finger E­box binding homeobox 2 (ZEB2), clathrin heavy chain (CLTC) and mediator complex subunit 1 (MED1) may be potential target genes of miR­205­5p. Reduced expression of miR­205­5p significantly increased the expression of ZEB2 mRNA and protein, inhibited the expression of erbB3 protein, but had no significant effect on the expression levels of CLTC and MED1. In summary, reduced expression of miR­205­5p promoted apoptosis and inhibited proliferation and invasion in lung cancer A549 cells through upregulation of ZEB2 and downregulation of erbB3. The present results suggested that the increased miR­205­5p expression observed in non­small cell lung cancer tissues may contribute to increased proliferation and invasion of lung cancer cells and thus to cancer progression.