Fig. 5: Acv3UTR-active YAP1 expression by absorbing miR-590-5p.

a Luciferase reporter assays. AGS or SGC7901 cells were cotransfected with the miR-590-5p sensor construct and pcDNA3.1-empty vector (EV) or different doses of pcDNA3.1-3ʹUTR. b Predicted biding sites of miR-590-5p in acv3UTR and mutant strategy. c MiR-590-5p expression level based on empty vector (EV), wild type 3ʹUTR, binding site 1 mutant type (MT1), binding site 2 mutant type (MT2) or dual sites mutant type (M3). d YAP1 level based on empty vector (EV), wild type 3ʹUTR, binding site 1 mutant type (MT1), binding site 2 mutant type (MT2) or dual sites mutant type (M3). e Cell localization of Acv3UTR, miR-590-5p, and YAP1 in AGS cells. f RIP was carried out using anti-Ago2 antibody in extraction of AGS cells. YAP1 (upper) and acv3UTR (lower) were enriched. g Mutation of Acv3UTR miR-590-5p binding site abolished promotion effects on AGS cells proliferation. *P < 0.05; **P < 0.01; ***P < 0.001 (paired t-test, two tailed).