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. 2018 Jun 20;16(3):3038–3044. doi: 10.3892/ol.2018.8999

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Copyright: © Jiang et al.

This is an open access article distributed 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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Figure 3. — ADAM9 is a direct target gene of miR-30a in RCC. (A) Sequence alignment of the wild-type and mutant 3′UTR of ADAM9, indicating the potential binding sites for miR-30a. (B) Luciferase reporter assays revealed a reduction in luciferase activities following the transfection of pMIR-ADAM9-3′UTR Wt into the 293T cells that overexpress miR-30a. (C) The exogenous expression of miR-30a suppressed ADAM9 mRNA expression in 786-O and A498 cells as determined by reverse transcription-quantitative polymerase chain reaction. (D) Ectopic expression of miR-30a inhibited the expression of ADAM9 protein in 786-O and A498 cells as determined using western blotting. *P<0.05 compared with the respective control. RCC, renal cell carcinoma; UTR, untranslated region; ADAM9, ADAM metallopeptidase domain 9; Wt, wild-type.