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. 2020 Mar 4;10(9):3952–3966. doi: 10.7150/thno.39578

Figure 7.

Figure 7

E2F1 activated transcription of miR-378a-3p. (A) Schematic representation of E2F1 binding site within the promoter of miR-378a-3p. (B) Increased mRNA levels of E2f1 in livers of HFD-treated mice (n=6) versus SD-treated mice (n=6). (C) Luciferase activities of miR-378a-3p promoter in Hepa1-6 cells transfected with miR-378a-3p promoter construct and E2f1 expression vector or empty vector (control). (D) No change was observed in luciferase activity of miR-378a-3p promoter with the mutated E2F1 binding site after E2f1 overexpression. (E) Increased levels of mature miR-378a-3p and pri-miR-378a in Hepa1-6 cells transfected with E2f1 expression vector or empty vector (control). (F) Reduced levels of mature miR-378a-3p and pri-miR-378a in Hepa1-6 cells transfected with MC-TTR-E2f1shRNA or empty vector (control). (G) In vivo ChIP assays were performed using genomic DNA isolated from livers of mice treated with SD and HFD; and the binding of E2F1 to the endogenous promoter of miR-378a-3p was detected using specific an E2F1 antibody. N.S: non-specific control using primers ∼10 kb downstream of miR-378a-3p promoter which served as negative control. Data represent mean ± SEM. **p < 0.01 (Student t test).