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. 2018 Nov 12;8(21):5890–5902. doi: 10.7150/thno.27667

Figure 6.

Figure 6

BPI-9016M increases miR203 and decreases DKK1. (A) miR103, miR203, miR200c, miR30b and miR30c expression levels by qPCR in A549 cells treated with BPI-9016M. U6 was used as the internal control. (B) Wound healing analyses of spreading miR203 inhibitor-transfected A549 and 1299 cells with BPI-9016M treatment. (C) Transwell assays to assess cell migration and invasion in miR203 inhibitor-transfected A549 and H1299 cells with or without BPI-9016M treatment. (D) Western blotting analyses demonstrating DKK1 expression in A549 and H1299 cells with miR103 or mi203 mimics (50 nM) and miR103 or miR203 inhibitors (50 nM). (E) The binding site of miR203 in the DKK1 3'-UTR is shown. 3'-UTR wild-type; 3'-UTR mutation and deletion sequences of the DKK1 3'-UTR. (F) Firefly luciferase activity between miR203 and wild-type, mutated, and deleted constructs of DKK1 3'-UTR. (G) Western blotting analysis showing DKK1 expression in A549 and H1299 cells with or without BPI-9016M/miR203 inhibitor. (H) A schematic illustration showing that BPI-9016M-inhibited proliferation, migration and invasion of lung adenocarcinoma is associated with ERK activation and miR203-DKK1-AKT signaling. (B-C, F) * p<0.05, ** p<0.001, *** p<0.0001.