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Fig. 2 | Molecular Cancer

Fig. 2

From: Bmi-1-induced miR-27a and miR-155 promote tumor metastasis and chemoresistance by targeting RKIP in gastric cancer

Fig. 2

miR-155 and miR-27a target RKIP, negatively regulate its expression, and promote the epithelial-mesenchymal transition (EMT) process. a The predicted binding site on the RKIP 3’UTR for miR-155 and miR-27a and the mutant sequence. b The relative luciferase activity of 293 T cells cotransfected with miRNAs and the indicated luciferase plasmid. *P < 0.05 vs. NC mimic, **P < 0.01 vs. NC mimic. c EMSA showed the formation of a stable dye-miR-27a/RKIP-Target complex, which was inhibited by the competitive interaction between excessive amounts of cold-miR-27a (unlabeled miR-27a) and RKIP-Target. d EMSA demonstrated no interaction between miR-155 and RKIP-Target. e The formation of a miR-27a/RKIP-Target protein complex by adding a cell cytoplasmic extract. f Western blot analysis showed the expression of RKIP and EMT-related marker genes after treatment with miR-155 mimic/inhibitor or miR-27a mimic/inhibitor. g Gene expression of RKIP and EMT-related marker genes modulated by miR-155 mimic/inhibitor or miR-27a mimic/inhibitor. *P < 0.05 vs. NC mimic, #P < 0.05 vs. NC inhibitor

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