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Fig. 4 | Journal of Experimental & Clinical Cancer Research

Fig. 4

From: β-Catenin nuclear localization positively feeds back on EGF/EGFR-attenuated AJAP1 expression in breast cancer

Fig. 4

AJAP1 interacted with β-catenin and mediated its nuclear location and transcriptional activity. a Co-IP assay results showed that AJAP1 formed a complex with β-catenin in T47D and MDA-MB-231 cells. b Co-IP assays showed that endogenous protein of AJAP1 interacted with β-catenin. c Western blot results showed that AJAP1 depletion increased nuclear translocation of β-catenin and overexpression of AJAP1 had the opposite function. d AJAP1-depleted stable cell lines were transfected with HA-Ub and then treated with MG132 as demonstrated. Cell lysates were subjected to β-catenin and showed that AJAP1-depletion inhibited the ubiquitination level of β-catenin. e AJAP1 reduced the β-catenin/TCF/LEF-mediated transcription activity in MDA-MB-231 and T47D cells with and without the upregulation of AJAP1. f AJAP1-depletion in MDA-MB-231 and T47D cells increased the β-catenin/TCF/LEF-mediated transcription activity. g-h overexpressed AJAP1 can reduce the protein (g) and mRNA(h) levels of β-catenin downstream genes as C-myc and CyclinD1 in MDA-MB-231 and T47D cells by western blot and RT-PCR. i-j AJAP1 knockdown can increase the protein (i) and mRNA(j) levels of β-catenin downstream genes, such as C-myc and CyclinD1 in MDA-MB-231 and T47D cells by western blot and qRT-PCR. Data were shown as mean ± SD. Each experiment was conducted in triplicate. **p < 0.01, ***p < 0.001

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