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. 2014 Sep;20(9):1431–1439. doi: 10.1261/rna.045757.114

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© 2014 Zhou and Rigoutsos; Published by Cold Spring Harbor Laboratory Press for the RNA Society

This article, published in RNA, is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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FIGURE 2. — MiR-103a-3p directly targets two sites in the 5′ UTR of GPRC5A. (A) The scheme indicates the sequences of the predicted miR-103a-3p binding sites (S11) within the 5′ UTR of GPRC5A and the sequences of S11 wild-type (WT, top) and mutant (MT, bottom) used in this study. (B) Luciferase activity in MIA PaCa-2 cells upon transfection of indicated reporter constructs and pre-miR-103a-3p were compared with cells transfected with indicated reporter constructs and pre-miR-scramble. (C) Luciferase activity in MIA PaCa-2 cells upon transfection of indicated reporter constructs and miR-103a-3p inhibitors was compared with cells transfected with indicated reporter constructs and Anti-miR-scramble. (D) Luciferase activity in MIA PaCa-2 cells upon transfection of indicated reporter constructs and pre-miR-103a-3p were compared with cells transfected with the indicated reporter constructs and pre-miR-scramble. (E) Luciferase activity in MIA PaCa-2 cells upon transfection of the indicated reporter constructs and miR-103a-3p inhibitors was compared with cells transfected with the indicated reporter constructs and Anti-miR-scramble. All numerical data are mean ± SD. (*) P < 0.05; (**) P < 0.01; (***) P < 0.001; n = 3. S11WT, psiCHECK-2 vector containing miR-103a-3p binding site 1; S11MT, psiCHECK-2 vector containing mutant miR-103a-3p binding site 1.