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Fig. 4 | Journal of Experimental & Clinical Cancer Research

Fig. 4

From: MAZ promotes prostate cancer bone metastasis through transcriptionally activating the KRas-dependent RalGEFs pathway

Fig. 4

MAZ transcriptionally activates RAS signaling. a The luciferase reporter activity of the NF-kB, TGF-β, EGFR, WNT, Notch and RAS pathway were analyzed in PC3 and VCaP. Luciferase reporter plasmids were employed to detect the activity of the NF-kB, TGF-β, EGFR, WNT, Notch and RAS pathways in PC-3 transfected with overexpression of MAZ or sh-MAZ plasmid, in VCaP transfected with si-MAZ plasmid. *P < 0.05. b Western blot analysis of HRas, KRas, NRas, p-ERK, activated RalA, p-AKT(S473), p-AKT(T308) in MAZ-overexpressing and MAZ-silencing cells. The total ERK, total RalA, and α-tubulin were used as a loading control. c,d The luciferase activity was monitored by transfection full-length HRas, KRas, or NRas promoter in vector, MAZ-overexpression, scramble, or MAZ-silencing PCa cells. Error bars represent such mean ± S.D. of three independent experiments. *P < 0.05. e, f Schematic illustration of the promoter regions of human KRas and HRas gene, and the regions containing the primers used for the ChIP assay (upper). ChIP was performed using an anti-MAZ antibody or a control IgG to identify MAZ binding sites in the KRas and HRas promoter. *P < 0.05.

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