Previous reports have indicated a potential link between microrna (mir)-214 and hypoxia. in the present study, the biological functions and potential mechanisms of mir-214 were determined, as well as its correlation with HiF-1α signaling in non-small cell lung cancer (nSclc) cells. Quantitative polymerase chain reaction revealed that mir-214 expression was upregulated in lung cancer tissues compared with adjacent normal tissues. mir-214 mimics were transfected into a549 cells, and MTT, colony formation, invasion and wound healing assays were performed. it was demonstrated that mir-214 mimic transfection promoted the invasion, proliferation and migration of a549 cells. Furthermore, mir-214 inhibitor transfection decreased H1299 cell invasion, proliferation and migration. next, the association between mir-214 expression and the HiF-1α signaling cascade was examined. it was demonstrated that mir-214 mimics upregulated the expression of hypoxia-inducible factor (HiF)-1α, vascular endothelial growth factor (VeGF), adenylate kinase 3 and matrix metalloproteinase (MMP)2, whereas mir-214 inhibitor downregulated the expression of these factors. using prediction software, it was demonstrated that tumor suppressor inG4 was a target of mir-214. a luciferase reporter assay confirmed that ING4 was a direct target of miR-214. There was a negative correlation between inG4 and mir-214 expression in lung cancer tissues. in addition, inG4 sirna and plasmid was transfected into cells in order to validate its effect on HiF-1α, MMP2 and VeGF expression. inG4 overexpression downregulated HiF-1α and its targets MMP2 and VeGF, while inG4 sirna upregulated HiF-1α, MMP2 and VeGF. in conclusion, it was demonstrated that mir-214 targeted inG4 in lung cancer cells, and upregulated the HiF-1α cascade, leading to MMP2 and VeGF upregulation. This approach may help to clarify the role of mirna in non-small lung cancer and may be a new therapeutic target for non-small lung cancer.