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. 2011 May 9;208(5):875–883. doi: 10.1084/jem.20110235

Figure 5.

Figure 5.

miR-200 and miR-192 family members regulate p53-mediated EMT by targeting ZEB1 and ZEB2. (A) p53+/+ and p53−/− RKO cells were transfected twice a week for 2 wk with indicated premiRs (50 nM). Cells were then photographed. A representative experiment out of three independent experiments is shown. (B) RKO (p53+/+ and p53−/−) cells transfected with indicated premiRs were subjected to in vitro invasion (top) and migration (bottom) assays. (C) C3A cells were transfected with luciferase constructs driven by 3′UTRs of ZEB1 or ZEB2 (RL-ZEB1, RL-ZEB2), together with scrambled miRNA inhibitor (Scr) or inhibitors of miR-141 (α-141) or miR-200c (α-200c). RL, Renilla luciferase; FL, Firefly luciferase. (D) RKO (p53+/+) cells were transfected with luciferase constructs driven by 3′UTRs of ZEB1 or ZEB2 (RL-ZEB1, RL-ZEB2), together with scrambled miRNA inhibitor (Scr) or inhibitors of miR-192 (α-192) or miR-215 (α-215). (E) Luciferase assay using C3A-sh-CTRL and C3A-sh-p53 cells transfected with pCIneo-hRL constructs containing ZEB1 or ZEB2 3′UTR with (200MUT) or without (WT) mutations in miR-200 family binding sites. (B-E) Data are mean ± SEM of three independent experiments and each is measured in triplicate (**, P < 0.05; *, P ≤ 0.01). Bars, 50 µm.