Skip to main content
. 2020 Mar 10;12(5):4506–4526. doi: 10.18632/aging.102904

Figure 6.

Figure 6

FOXO1 acted as the direct target of miR-223-3p. (A) Bioinformatics programs assay revealed complementary binding within miR-223-3p and FOXO1 3’UTR. (B) The luciferase reporter constructs containing WT-FOXO1 or MU-FOXO1 sequence. (C) Dual-luciferase reporter assay verified the targeting relationship between miR-223-3p and FOXO1. (D) Relative quantification of mRNA levels of FOXO1. Three independent experiments were performed. (E) Tube formation assay showing the angiogenesis ability of EPCs by FOXO1 knockdown and overexpression. Scale bar=200μm. (original magnification, ×100). FOXO1 knockdown and overexpression, respectively, repressed and enhanced capability of angiogenesis in EPCs. (F) Effects of FOXO1 on cell migration were analysed by wound healing assay. Scale bar=200μm. (original magnification, ×100). FOXO1 knockdown and overexpression, respectively, reduced and increased number of EPCs migrated. (G) Transwell invasion assay showed that FOXO1 knockdown and overexpression, respectively, inhibited and promoted the ability of cell invasion in EPCs. Scale bar=100μm. (original magnification, ×200). **P < .01, ***P < .001 compared to NC group. Data are represented as mean ± SEM.