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. 2018 Jan 26;9(2):130. doi: 10.1038/s41419-017-0131-3

Fig. 5. miR-874-DOR induced inhibition of proliferation and migration through EGFR–ERK pathway.

Fig. 5

a Levels of the DOR, phosphorylated PKC, and phosphorylated ERK were detected using Western blot analysis. miR-874-overexpressed cells were treated with 20 ng/ml of EGF or combined with 10 µM of U1026. b, c Ratios of density units for each phospho- to total-protein are shown. Phosphorylation of the EGFR and ERK were downregulated by miR-874 overexpression, and ectopic DOR expression eliminated the promoting effect of miR-874 overexpression on phosphorylation level. The EGF significantly restored inhibition of phosphorylation of the EGFR and ERK induced by miR-101 overexpression. When miR-874-overexpressed SK-hep-1 cells were treated with EGF combined with U1026, EGF-induced phosphorylation of ERK was blocked without interfering with EGFR phosphorylation. d The proliferation-promoting effect of the EGF on miR-874-overexpressing SK-hep-1 cells was blocked by U1026, as demonstrated by an MTT assay. e The invasion-promoting effect of the EGF was blocked by U1026, as demonstrated by transwell assay. f The migration-promoting effect of the EGF was blocked by U1026, as demonstrated by wound-healing assay. Data are shown as the mean ± SD of three replicates (*p < 0.05)