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. 2016 Jul 13;7(32):52340–52353. doi: 10.18632/oncotarget.10566

Figure 5. Hsa-miR-184 targets the AKT2/mTOR pathway, and inhibits cell proliferation and migration.

Figure 5

A. Schematic construction of reporter containing a fragment of the wild type and mutant AKT2 3′-TUR. B. Relative luciferase activities were measured in ARPE-19 cells. Renilla luciferase vector was used as an internal control. C. mRNA expression of AKT2 were analyzed in 30 dpd hiPSC-RPE transfected with NC mimic or hsa-miR-184 mimic, respectively. D. AKT2 levels were determined in hiPSC-RPE at 30, 60, and 90 dpd. E-F. AKT2 expression was elevated in ARPE-19 cells transfected with AcFlag-AKT2 (E), and was suppressed in cells transfected with AKT2-siRNA (F). G-H. Relative mRNA expressions of MITF, RPE65, RLBP1, LRAT, BEST1, KRT18, and CTNNB1 in hiPSC-RPE at 30 dpd transfected with hsa-miR-184 mimic plus empty expression vector compared to hsa-miR-184 mimic plus AcFlag-AKT2 (G), and in cells transfected with hsa-miR-184 inhibitor plus scramble siRNA compared hsa-miR-184 inhibitor plus AKT2-siRNA (H). *: p<0.05; **: p<0.01; ***: p<0.001.