Fig. 5

AJAP1 regulated tumor progression by regulating β-catenin in breast cancer a Validation of protein levels of three groups after transfected with related shRNA by Western Blot b、d Results of the transwell assay (b) and wound-healing assay(d) showed that AJAP1/β-catenin KD inhibited invasion and migration abilities of T47D cell, indicating that β-catenin can reverse the effect of AJAP1-depletion caused (Transwell assay: original magnification, × 200). c、e MTT(c) and Colony-forming assay(e) were conducted to determine the clone-initiating and proliferation ability among AJAP1 KD, AJAP1/β-catenin KD and control in T47D cells. f Flow cytometry results of AJAP1 KD, AJAP1/β-catenin KD and control in T47D cells. g Representative images of tumor isolated from three groups (left panel) as demonstrated and tumor growth (middle panel), tumor weight representative graph(right) h H&E staining of tumors isolated from three experimental groups (magnification, × 400), IHC staining of Ki67, C-myc and CyclinD1 in slides removed from the three groups (magnification, × 400) and typical images of micrometastasis of the lung and liver (magnification, × 100). i Corresponding analysis of the positive rates of Ki67, C-myc and CyclinD1 expression in three groups(top), the number of liver and lung micrometastasis in three related groups. Data were shown as mean ± SD. Each experiment was conducted in triplicate. **p < 0.01, ***p < 0.001