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. 2019 Dec 27;19:354. doi: 10.1186/s12935-019-1060-2

Fig. 5.

Fig. 5

miR-100-3p functioned through BMPR2 in inhibiting Smad1/5/9、ERK-AKT and Bcl-2 signaling. a Western blotting for Smad1/5/9, p-smad1/5/9, Bcl-2, Bax, Caspase3, ERK1/2, p-EKR1/2, AKT and p-AK in AGS cells transfected with Lv-miR-100-3p mimic-control (Lv-miR-100-3p mimic-ctrl) and over-expression BMPR2 plasmid control(over-expression BMPR2 control-ctrl), Lv-miR-100-3p mimic-ctrl and over-expression BMPR2 plasmid, Lv-miR-100-3p mimic and over-expression BMPR2-ctrl, or Lv-miR-100-3p mimic and over-expression BMPR2 plasmid. b MGC-803 cells transfected with Lv-miR-100-3p inhibitor-control (inhibitor-ctrl) and BMPR2 shRNA control (shRNA-ctrl), Lv-miR-100-3p inhibitor-ctrl and BMPR2 shRNA, Lv-miR-100-3p inhibitor and BMPR2 shRNA-ctrl, or Lv-miR-100-3p inhibitor and BMPR2 shRNA. Protein expression was quantified by band intensity and normalized to β-actin. **p < 0.01