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. 2015 Sep 1;106(9):1143–1152. doi: 10.1111/cas.12730

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© 2015 The Authors. Cancer Science published by Wiley Publishing Asia Pty Ltd on behalf of Japanese Cancer Association.

This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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MiR-214 targets the EGFR signaling inhibitor Mig-6. (a) Sequence alignment of putative binding sites of miR-214 in the 3′-UTR sequence of Mig-6 and the construction of the reporter plasmid (pmirGLO-Mig-6). (b) Locked nucleic acid (LNA)-antimiR-214 significantly increased the luciferase activity of pmirGLO-Mig-6, a reporter plasmid containing the putative binding site of miR-214 in the 3′-UTR of Mig-6, while mimic-214 decreased the luciferase activity of pmirGLO-Sema6A (n = 6). (c) Changes in the expression of Mig-6 in the liver of Pdgf-c Tg mice that were injected with saline, LNA-antimiR-control or LNA-antimiR-214 (n = 5). (d) Western blotting of EGFR-related genes in the liver of Pdgf-c Tg mice that were injected with saline, LNA-antimiR-control or LNA-antimiR-214. All experiments were performed in duplicate and repeated three times. *P < 0.05, **P < 0.01, ***P < 0.001, Values are means ± SD.