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Fig. 5 | Journal of Experimental & Clinical Cancer Research

Fig. 5

From: Melanoma cell-secreted exosomal miR-155-5p induce proangiogenic switch of cancer-associated fibroblasts via SOCS1/JAK2/STAT3 signaling pathway

Fig. 5

MiR-155 targets 3′UTR of SOCS1. a The wild-type and a mutated type of binding site between miR-155 and SOCS1. b, c Overexpression of miR-155 reduced SOCS1–3′UTR luciferase activity in vitro but not mutated SOCS1–3′UTR luciferase activity. Inhibition of miR-155 resulted in the opposite effect. d, e Western blot and densitometry analysis showed that overexpression of miR-155 suppressed the expression of SOCS1 in NIH/3T3 cells. * P < 0.05, ** P < 0.01. Student’s t-tests. Independent experiments performed in triplicate. Values are expressed as means ± SEM. Anti-NC: inhibitor negative control. Anti-miR-155: miR-155 inhibitor. GAPDH: Glyceraldehyde 3-phosphate dehydrogenase. MiR-NC: miR-negative control. Mut: mutated type. SEM: standard error of the mean. SOCS1: suppressor of cytokine signaling 1. WT: wild type. 3′UTR: 3′ untranslated region

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