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. 2015 Mar 10;4(3):e231. doi: 10.1038/mtna.2015.5

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Copyright © 2015 American Society of Gene & Cell Therapy

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AKT1 is a direct target of miR-4689 in mutant KRAS CRC cells. (a) ERK phosphorylation was similar in DLD1 KRAS^G13D cells treated with miR-4689, siMEK1, or siMEK2 (25 nM). (b) Proliferation of mutated KRAS DLD1 cells was significantly suppressed by miR-4689 compared to siMEK1 or siMEK2 (P < 0.01 and P < 0.05, respectively, two-way ANOVA). (c) Sequence alignment of miR-4689 with the coding sequence (CDS) of human AKT1 shows complementary nucleotide binding sites (dotted lines). (d) Luciferase activity of the AKT1 CDS reporter in the presence of 50 nM of miR-4689 or miR-NC. (e) Immunoblots and (f) qRT-PCR results show AKT1 expression in SW480 KRAS^G12V and DLD1 KRAS^G13D cells treated with miR-NC or miR-4689. ACTB was the housekeeping control. All data represent mean ± SEM.