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. 2021 Oct 14;12(10):948. doi: 10.1038/s41419-021-04253-y

Fig. 7. CircNPHP4 promoted the EGFR/PI3K/AKT pathway through miR-1231.

Fig. 7

CircNPHP4 promoted the EGFR/PI3K/AKT pathway through miR-1231 inhibition in HCAECs qRT-PCR quantification of EGFR and CACNA2D2 expression after miR-1231 overexpression (A) or circNPHP4 knockdown (B). EGFR and CACNA2D2 expression after transfection with miR-1231 inhibitor (C) or circNPHP4 expression vector (D) was quantified with qRT-PCR. Luciferase assay where HCAEC were co-transfected with a scrambled control, circNPHP4 expression plasmid, and a luciferase reporter plasmid containing either wild-type EGFR (EGFR-WT) or an EGFR construct with mutated miR-1231 binding sites (EGFR-mut) (E). F–I Reversion assays using vectors overexpressing or knocking down circNPHP4, as well as miR-1231 mimics or inhibitors. Data are presented as means ± SD; a significant difference was identified with Student’s t test. *P < 0.05; **P < 0.01; ns (not significant). J A proposed model illustrating the role of monocyte-derived sEVs circNPHP4 in regulating heterogeneous adhesion in vein endothelial cells.