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Fig. 5 | Journal of Experimental & Clinical Cancer Research

Fig. 5

From: Activation of EGFR-DNA-PKcs pathway by IGFBP2 protects esophageal adenocarcinoma cells from acidic bile salts-induced DNA damage

Fig. 5

IGFBP2 is required for acidic bile salts-induced EGFR nuclear accumulation to activate DNA-PKcs in EAC cells. a, FLO1 cells were treated with acidic bile salts (ABS, pH 4, 200 μM) for 20 min and recovered for 0.5 h and 3 h. Cytoplasmic and nuclear fractions were analyzed using western blot analysis. Data shows that ABS induces IGFBP2 nuclear translocation as well as accumulation of p-EGFR. b, FLO1 cells with IGFBP2 knockdown (si-IGFBP2) and control cells were treated with ABS for 20 min and recovered for 0.5 h. Cytoplasmic and nuclear fractions were analyzed by using western blot analysis. Data displays attenuated nuclear accumulation of IGFBP2, p-EGFR, and p-DNA-PKcs, following knockdown of IGFBP2 and ABS treatment. c, FLO1 cells with IGFBP2 knockdown and control cells were treated with ABS for 20 min and recovered for 0.5 h. Immunofluorescence staining for IGFBP2 (red) and EGFR (green) was performed. DAPI (blue) was used to stain the nuclei. d, FLO1 cells were treated with EGFR tyrosine kinase inhibitor, gefitinib (10 μM) for 24 h. Then cells were exposed to ABS for 20 min and recovered for 0.5 h. Cytoplasmic and nuclear fractions were analyzed by using western blotting. e, OE33 cells with IGFBP2 overexpression were treated with and without EGFR tyrosine kinase inhibitor, gefitinib (10 μM) for 24 h. Then cells were treated with ABS for 20 min and recovered for 3 h. Cytoplasmic and nuclear fractions were analyzed by using western blotting

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