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. 2018 Oct 9;17(16):1949–1966. doi: 10.1080/15384101.2018.1496741

Figure 4.

Figure 4.

AFAP1-AS1 acts as a ceRNA for miR-133a in PC cells. (a) Schematic representation of the predicted target site for miR-133a in AFAP1-AS1. (b) Relative expression levels of miR-133a in 63 paired cancerous and peritumoral normal tissues. p < 0.01 vs. Normal tissue group. (c) Relative expression levels of miR-133a in pancreatic cancer cells (AsPC-1, BxPC-3, PANC-1, PaCa-2 and SW1990) and primary cultures of normal human pancreatic duct epithelial cells (HPDE6c7) used as a control. Data are represented as the mean ± S.D. from three independent experiments, *p < 0.05, **p < 0.01 vs. HPDE6c7. (d) Relative expression level of miR-133a in PaCa-2 and SW1990 cells after siRNA transfection. Data are represented as the mean ± S.D. from three independent experiments, **p < 0.01 vs. si-Scramble. (e) Relative expression level of miR-133a in PaCa-2 and SW1990 cells after Lv-AFAP1-AS1 infection. Data are represented as the mean ± S.D. from three independent experiments, **p < 0.01 vs. Lv-control. (F) The Spearman’s rank test was used to analyze the relationship between AFAP1-AS1 and miR-133a expression levels in PC tissues (r:-0.7610, p < 0.01). (g) Luciferase reporter assay in human embryonic kidney (HEK) 293T cells, co-transfected with the reporter plasmid (or the corresponding mutant reporter) and the indicated miRNAs. miR-133a mimics significantly decreased the luciferase activity in wt-AFAP1-AS1 but not in mut-AFAP1-AS1. Data are represented as means ± S.D. from three independent experiments, **p < 0.01 vs. mimics NC.