miR‐214 mediates vascular smooth muscle cell (VSMC) growth and motility by modulating NCK associated protein 1 (NCKAP1). VSMCs were cotransduced with miR‐214 inhibitor, NCKAP1 short hairpin RNA (shRNA) lentivirus (NCKAP1 sh), and/or respective controls (control microRNA [miRNA] or nontarget shRNA [nontarget]), as indicated. Transduced cells were serum‐starved for 24 hours and subjected to reverse transcriptase–quantitative PCR analyses to examine miR‐214, NCKAP1, and proliferating cell nuclear antigen (PCNA) expression levels (A), cell counting (B), immunofluorescence staining with antibody against Ki‐67 (C1 and C2), transwell migration (D1 and D2), and F‐actin staining using phalloidin‐FITC (E) in response to serum (A through C and E) or 30 ng/mL platelet‐derived growth factor BB (D) stimulation. The data presented are representative images (C2, D2 and E) or mean+SEM (A, B, C1 and D1) of 3 independent experiments. *<0.05, **<0.01, ***<0.001 (Compared various treatments with double control), #<0.05 (Compared NCKAP1 knockdown with control in VSMCs with miR‐214 inhibition).