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. 2017 Jul 10;6(7):e356. doi: 10.1038/oncsis.2017.59

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Copyright © 2017 The Author(s)

Oncogenesis is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 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/4.0/

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MiR-137 directly targets ASCT2 3′-UTR. (a) Base-pair binding between miR-137 and putative miRNA-binding sites within ASCT2 3′-untranslated regions (UTRs) across different species. (b, c) MiR-137 mimics selectively reduced ASCT2 mRNA (b) and protein (c) levels in tumor cells from different cancer types. Actin was used as a loading control. Mean±s.d. (n=3), t-test; **P<0.01. (d, e) Luciferase assays of human ASCT2 3′-UTR constructs with intact and mutated seed sequences for miR-137 in 293 T (d) and HCT116 (e) cells. Mean±s.d. (n=3), t-test; *P<0.05.