Research Paper Volume 11, Issue 15 pp 5705—5725

Figure 4. ADAMTS9-AS2 overexpression and miR-27a-3p knockdown inhibit ccRCC cell proliferation. (A) 786-O and caki-1 cells transfected with pcDNA ADAMTS9-AS2 exhibited decreased proliferation compared to those with pcDNA control, based on the MTS assay. (B) 786-O and caki-1 cells transfected with miR-27a-3p exhibited increased proliferation compared to cells transfected with NC, based on the MTS assay. (C) 786-O and caki-1 cells transfected with si-ADAMTS9-AS2 displayed preferable proliferation compared to cells transfected with NC, based on the MTS assay. (D) 786-O and caki-1 cells transfected with miR-27a-3p inhibitor exhibited decreased proliferation compared to cells transfected with NC, based on the MTS assay. (E) Colony formation and crystal violet staining assays were performed in 786-O and caki-1 cells transfected with pcDNA control or pcDNA ADAMTS9-AS2, or (F) in 786-O and caki-1 cells transfected with NC or miR-27a-3p inhibitor. ADAMTS9-AS2 overexpression and miR-27a-3p knockdown significantly repressed colony formation of ccRCC cells. Scale bar = 100 μm. Three independent experiments were performed and data shown are mean ± SD. Statistically significant differences are indicated as *, P<0.05, **, P<0.01; Student’s t-test. ADAMTS9-AS2, ADAM metallopeptidase with thrombospondin type 1 motif, 9 antisense RNA 2; miR-27a-3p, microRNA-27a-3p; MTS, (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfop-henyl)-2H-tetrazolium); si, small interfering; NC, negative control; ccRCC, clear cell renal cell carcinoma; SD, standard deviation.