Figure 4.

Overexpression of miR-181a promotes the migration, proliferation and inhibitors apoptosis of ESCC cells although downregulation of miR-181a shows the opposite effects. ECA109 and TE-1 cells were transfected with mimics, inhibitor and negative control. Cells were divided into four groups: miR-181a mimics, mimics NC, miR-181a inhibitor and inhibitor NC. (A) The relative expression of miR-181a of ECA109 was assessed using RT-qPCR 48 h after transfection. (B) The relative expression of miR-181a of TE-1 was assessed using RT-qPCR 48 h after transfection. (C) The migration abilities of ECA109 cells were detected by wound healing assays (magnification, ×100). (D) The migration abilities of TE-1 cells were detected by wound healing assays (magnification, ×100). (E) The proliferation of ECA109 cells was determined by the CCK-8 assay. (F) The proliferation of TE-1 cells was determined by the CCK-8 assay. (G) The apoptosis rate of ECA109 cells was measured by flow cytometry. (H) The apoptosis rate of TE-1 cells was measured by flow cytometry. The date is expressed at the means ± standard deviation (n=3) of one representative experiment. *P<0.05, **P<0.01, ***P<0.001. miR, microRNA; ESCC, esophageal squamous cell carcinoma; NC., negative control; RT-qPCR, reverse transcription-quantitative PCR; OD, optical density; PI, propidium iodide.