Fig. 7

AKT is the downstream effector of SET and relationship of lncRNA with, miR-502-3p, SET and p-AKT in GBC. a Western blot assays of SET, p-AKT and AKT expression in shcontrol- or sh-HGBC-expressing NOZ or SGC-996 cells. b Western blot assays of SET, p-AKT and AKT expression in pcDNA3.1-based vector control and lncRNA-HGBC-expressing GBC-SD and EH-GB1 cells. c Western blotting analysis of N-cadherin, Vimentin, p-AKT and AKT expression in GBC-SD (left) and EH-GB1 (right) cells. d Western blotting analysis of N-cadherin, Vimentin, SET, p-AKT and AKT expression in indicated cells. e The expression of N-cadherin, vimentin, phosphorylated AKT and AKT was determined in GBC-SD and EH-GB1 cells in presence or absence of 10 uM MK2206. tubulin was used as the loading control. f The correlation between lncRNA-HGBC and SET (upper left), miR-502-3p (upper right) or HuR (bottom) expression was detected in 43 GBC specimens by qRT–PCR. The ΔCt values were subjected to Pearson correlation analysis. g Representative images of SET (top) or p-AKT (bottom) expression by immunohistochemical staining from non-tumor tissues and GBC tumors. Scale bars, 100 μm. h-i Scatterplots of the average staining scores for SET (h) or p-AKT (i) expression in GBC patients with low or high expression of lncRNA-HBC. j Schematic diagram of lncRNA-HGBC functions to promote tumor growth and metastasis in GBC cells