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. 2018 Aug 16;10(8):272. doi: 10.3390/cancers10080272

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© 2018 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Suppression of CCNG2 by miR-1246 contributes to oral cancer stemness. (A) Schematic presentation of the constructed CCGN2 3′UTR reporter plasmids. Wild-type and mutated (Mut) CCNG2 reporter plasmids were co-transfected with miR-1246 or empty vectors; (B) The luciferase activity of each combination was assessed and showed that only WT reporter activity was inhibited by miR-1246; (C) CCNG2 protein expression in OSCC lines was examined by western blotting; (D) The relationship between miR-1246 and CCNG2 expression was shown; (E) Self-renewal, (F) migration, (G) colony-formation capacities of cells transfected with miR-1246 inhibitor with or without silence of CCNG2 were evaluated. * p < 0.05 compared with control group; ^# p < 0.05 compared with miR-1246 inhibitor only group.