Research Paper Volume 11, Issue 15 pp 5705—5725

Figure 5. ADAMTS9-AS2 overexpression and miR-27a-3p knockdown decrease ccRCC cell chemoresistance to 5-Fu. (A) MTS assays were performed in 786-O and caki-1 cells transfected with pcDNA control or pcDNA ADAMTS9-AS2 and treated with the indicated concentrations of 5-Fu. (B) MTS assays were performed in 786-O and caki-1 cells transfected with NC or miR-27a-3p inhibitor and treated with the indicated concentrations of 5-Fu. (C) MTS assays were performed in 786-O and caki-1 cells transfected with NC or si-ADAMTS9-AS2 and treated with the indicated concentrations of 5-Fu. (D) MTS assays performed in 786-O and caki-1 cells transfected with NC or miR-27a-3p and treated with the indicated concentrations of 5-Fu. (E) Expression levels of ADAMTS9-AS2 and (F) miR-27a-3p were determined by qRT-PCR in 5-Fu-resistant 786-O and caki-1 cells. 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; ccRCC, clear cell renal cell carcinoma; MTS, (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfop-henyl)-2H-tetrazolium); si, small interfering; NC, negative control; qRT-PCR, quantitative real-time polymerase chain reaction; SD, standard deviation.