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Fig. 5 | Experimental Hematology & Oncology

Fig. 5

From: ASAP2 interrupts c-MET-CIN85 interaction to sustain HGF/c-MET-induced malignant potentials in hepatocellular carcinoma

Fig. 5

ASAP2 triggers the epithelial-mesenchymal transition (EMT) in hepatocellular carcinoma (HCC). A Gene set enrichment analysis (GSEA) results indicated that EMT-related molecular signatures were significantly enriched in ASAP2-high HCC samples according to The Cancer Genome Atlas (TCGA) dataset. B Expression levels of N-Cadherin and E-Cadherin in ASAP2-knockdown SNU182 cells, ASAP2-knockdown SNU387 cells, ASAP2-overexpression Hep3B cells and their corresponding control cells were evaluated by immunofluorescence staining. C Effects of ASAP2 knockdown (left) or ASAP2 overexpression (right) on the protein expression levels of EMT-related markers in HCC cells were determined by western blot (WB) assays. D Protein expression levels of EMT-related markers in HCC tissues derived from mice models generated by transplanting shControl or shASAP2-SNU182/SNU387 cells were assessed by WB assays. E Protein expression levels of EMT-related markers in frozen HCC samples with distinct ASAP2 states were determined by WB assays. F Expression patterns of N-Cadherin and E-Cadherin in patients with distinct ASAP2 states in clinical HCC samples were determined by immunohistochemistry staining. G Associations between ASAP2 and EMT-related markers such as N-Cadherin, Vimentin, and Snail1 according to TCGA Liver hepatocellular carcinoma (LIHC) cohort and the Gene Expression Profiling Interactive Analysis (GEPIA) dataset

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