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. 2017 Jul 31;36(47):6518–6530. doi: 10.1038/onc.2017.257

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Copyright © 2017 The Author(s)

This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/4.0/

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TEAD1 and TEAD4 are direct targets of miR-377-3p, miR-1343-3p and miR-4269. (a) Putative binding sites in 3′-UTR of TEAD1 or TEAD4 for the related miRNA binding. (b) mRNA expression of TEAD1 and TEAD4 in MGC-803 and SGC-7901 cells after ectopic expression of miR-377-3p, miR-1343-3p and miR-4269 (*P<0.05; **P<0.001; unpaired t-test). (c) Western blot analysis of TEAD1 and TEAD4 when overexpression of miR-377-3p, miR-1343-3p and miR-4269 in MGC-803 and SGC-7901 cells. (d) Both miR-377-3p and miR-4269 suppressed the relative luciferase activity of constructs encompassing the binding sites in TEAD1 3′-UTR. Meanwhile, after ectopic expression of miR-1343-3p or miR-4269, the luciferase activities were also inhibited in the constructs containing the wild-type binding sites in TEAD4 3′-UTR (**P<0.001; unpaired t-test).