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. 2019 Dec 31;19(3):1806–1816. doi: 10.3892/etm.2019.8406

Figure 5.

Figure 5.

Figure 5.

Effects of AMACR and miR200c on cell migration and invasion. (A) Wound-healing assay images and (B) quantitative analysis. si-knockdown of AMACR or overexpression of miR200c by Ad-miR200c inhibited wound-healing in DU145 and PC-3 cells. Restoration of AMACR using pcDNA3.1-AMACR reversed those inhibitory effects. (C) Transwell assay images and (D) quantitative analysis. Si-knockdown of AMACR or overexpression of miR200c by Ad-miR200c inhibited migration and invasiveness of the prostate cancer cells, whereas overexpression of AMACR reversed this inhibition. All experiments were performed in triplicate. Data are presented as the mean ± standard deviation. *P<0.05 and **P<0.01 vs. si-Control, #P<0.05 and ##P<0.01 vs. Ad-miR200c. AD, adenovirus; AMACR, α-methylacyl coenzyme A racemase; siRNA, small interfering RNA; miR, microRNA.