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Fig. 3 | Journal of Experimental & Clinical Cancer Research

Fig. 3

From: miR-221 stimulates breast cancer cells and cancer-associated fibroblasts (CAFs) through selective interference with the A20/c-Rel/CTGF signaling

Fig. 3

c-Rel is involved in the up-regulation of the CTGF triggered by miR-221. a CTGF mRNA levels in CAFs, MDA-MB 231 and SkBr3 cells transfected for 48 h with 25 nM miR-Ctrl and 25 nM miR-221, alone or in combination with 100 nM LNA-i-miR-221 (LNA-i). Data are shown as fold changes respect to the scrambled controls. b CTGF mRNA levels in CAFs, MDA-MB 231 and SkBr3 cells transfected for 8 h with shRNA or shRel and then transfected for 48 h with 25 nM miR-221. Data are shown as fold changes respect to the scrambled controls. CTGF protein levels in CAFs (c), MDA-MB 231 (d) and SkBr3 (e) cells transfected for 48 h with 25 nM miR-Ctrl and 25 nM miR-221, alone or in combination with 100 nM LNA-i-miR-221 (LNA-i). β-actin serves as a loading control. Below panels show densitometric analysis of the blots normalized to the loading controls. CTGF protein levels in CAFs (f), MDA-MB 231 (g) and SkBr3 (h) cells transfected for 8 h with shRNA or shRel and then transfected for 48 h with 25 nM miR-221. β-actin serves as a loading control. Below panels show densitometric analysis of the blots normalized to the loading controls. Efficacy of c-Rel silencing in CAFs (i), MDA-MB 231 (j) and SkBr3 (k) cells. β-actin serves as a loading control. Side panels show densitometric analysis of the blots normalized to the loading controls. Results shown are representative of at least three independent experiments. (**) indicates p < 0.01

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