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Fig. 5 | Journal of Experimental & Clinical Cancer Research

Fig. 5

From: EphA1 activation promotes the homing of endothelial progenitor cells to hepatocellular carcinoma for tumor neovascularization through the SDF-1/CXCR4 signaling pathway

Fig. 5

EphA1 increases SDF-1 expression via activation of the Akt and mTOR pathways. a WB assay of the EphA1 downstream signaling molecules ERK, AKT and mTOR, expressed in untreated and treated HLE cells as well as Huh-7 cells with manipulated EphA1 levels, with β-actin as a control or protein loading. b Histograms show the relative (Rel) protein expression results from WB, which were normalized to the expression level in untreated cells. The data represent the mean ± SD of three independent experiments. Asterisks indicate significant differences (**P < 0.01; ***P < 0.001), and “ns” indicates an insignificant difference. c The WB assay of SDF-1 in IgG-Fc- or ephrinA1-Fc-activated HLE cells after the respective blockage of the Akt and mTOR pathways with the corresponding specific inhibitors LY294002 (2 ng/ml) and rapamycin (2 ng/ml). Β-actin served as a control for protein loading. The data represent the mean ± SD of three independent experiments. Asterisks indicate significant differences (**P < 0.01) d Double IF staining of SDF-1 (green) and EphA1 (blue). Images were obtained using a confocal laser scanning microscope. The results show that SDF-1 expression decreases after the blockage of the Akt and mTOR pathways with their respective specific inhibitors, LY294002 (2 ng/ml) and rapamycin (2 ng/ml). Magnification: × 400; scale bar: 10 μm

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