Skip to main content
. 2017 Jan 4;19(5):648–659. doi: 10.1093/neuonc/now251

Fig. 5.

Fig. 5

CECR1 function in macrophages activates the MAPK pathway in U87 cells. (A) Western blot of phospho-ERK1/2 and total ERK1/2 in U87 cells at 10 and 20 minutes after stimulation with MΦ-CM from siSham and siCECR1 transfected macrophages. (B) Phospho-ERK/total ERK ratios are presented as mean ± SEM in fold change compared with MΦ-CM derived from macrophages with nontargeted siRNA (siSham) and siRNA targeting CECR1 (siCECR1) from 5 experiments. *P < .05. (C) Western blot of phospho-JNK/SAPK and total JNK/SAPK protein in U87 cells at 10 and 20 minutes after stimulation with MΦ-CM derived from siSham and siCECR1 transfected macrophages. (D) Phospho-JNK/total JNK ratios are presented as mean ± SEM in fold change compared with MΦ-CM derived of macrophages with non-targeted siRNA (siSham) and siRNA targeting CECR1 (siCECR1) from 3 experiments. *P < .05. (E) Western blot of phospho-/total c-Jun in U87 cells at 10 and 20 minutes after stimulation with MΦ-CM derived from siSham and siCECR1 siRNA transfected macrophages. (F) Phospho–c-Jun/total c-Jun ratios at 20 minutes after stimulation are presented as mean ± SEM in fold change compared with MΦ-CM derived from macrophages with nontargeted siRNA (siSham) and siRNA targeting CECR1 (siCECR1) from 3 experiments. *P < .05. (G) Representative immunostainings of phospho–c-Jun in U87 cells of 2 experiments. U87 were stimulated with MΦ-CM derived from siSham and siCECR1 transfected macrophages for 15 and 30 minutes (scale bar: 100 µm). (H) Quantified phospho–c-Jun in U87 cells were obtained from 200 randomly selected cells and presented as mean ± SEM in each condition. **P < .01, ***P < .005.