Research Paper Volume 13, Issue 17 pp 21232—21250

Figure 2. Upregulation of SNHG17 drives malignant phenotype of RCC. (A) qRT-PCR assay analysis of the expression of SNHG17 in 786-O and ACHN cell lines transfection with pcDNA3.1/SNHG17 or pcDNA3.1. (B–C) CCK-8 assay (B) and Cell Titer-Glo Luminescent cell viability assay (C) analysis of the proliferative ability of 786-O and ACHN cells transfected with the indicated vectors. (D) The activity of caspase-3, -8, and -9 assay analysis of cell apoptosis of786-O and ACHN cells transfected with the indicated vectors. (E) The wound healing assay analysis of cell migration in 786-O and ACHN cell lines transfected with the indicated vectors. (F) The transwell assay analysis of cell migration and invasion in 786-O and ACHN cell lines transfected with the indicated vectors. (G) SNHG17 overexpression remarkably increased the volume and weight of tumor xenograft. Scale bar, 1.0 cm. (H) qRT-PCR assay analysis of expression of SNHG17, H2AX and miR-328-3p in the tumor xenograft. (I) Immunohistochemistry staining of Ki-67 in the tumor xenograft. Scale bar, 200 μm. Data are presented as means ± standard deviation from triplicate experiments. A t-test was used to evaluate the statistical significance as compared to the control. RCC, renal cell carcinoma. ^*P < 0.05; ^**P < 0.01; ^***P < 0.001.