Fig 1: Up-regulation of SSAT inhibited AKT/GSK3β/β-catenin signaling pathway and Epithelial-to-Mesenchymal transition in hepatocellular and colorectal carcinoma cellsA. Western blot analysis demonstrated that the protein expression of p-AKT, AKT and p-GSK3 was decreased in HepG2, SMMC7721 and HCT 116 cells transfected with SSAT compared with the cells without transfection or transfected with Vector. β-actin was used as an internal control. B, C. Western blot analysis showed the expression of β-catenin (total and nucleus protein), cyclin D1, N-cadherin, Slug and Twist1 were decreased in SMMC7721, HepG2 and HCT 116 cells transfected with SSAT compared with the cells without transfection or transfected with Vector. The epithelial marker E-cadherin was increased in HepG2, SMMC7721 and HCT 116 cells transfected with SSAT compared with the cells without transfection or transfected with Vector. Lamin B1 was used as an internal control of nucleus protein, β-actin was used as an internal control of total protein.
Fig 2: SNAI2 promotes the proliferation of GSCs.A The overexpression and knockdown efficiency of SNAI2 in GSCs validated with RT-qPCR. B The overexpression and knockdown efficiency of SNAI2 in GSCs as detected by Western blot assay. C Statistics of EdU-positive cells in GSCs. D Statistics of cell sphere formation efficiency of GSCs. E The proliferation of GSCs in response to oe-NC, oe-SNAI2, si-NC or SNAI2-KD as detected by EdU assay. F The sphere-forming ability of GSCs in response to oe-NC, oe-SNAI2, si-NC or SNAI2-KD as examined by spheroid formation assay. G the apoptosis of GSCs in response to oe-NC, oe-SNAI2, si-NC, or SNAI2-KD as examined by flow cytometry. *p < 0.05 vs. GSCs treated with oe-NC or si-NC. Each cell experiment was repeated three times independently.
Fig 3: SNAI2 promotes in vivo tumorigenesis of glioma by inhibiting the PHLPP2 to activate the Akt pathway.A The weight of tumor xenografted in nude mice in the presence of oe-NC, oe-SNAI2, oe-PHLPP2, or oe-SNAI2 + oe-PHLPP2. B The volume of tumor xenografted in nude mice in the presence of oe-NC, oe-SNAI2, oe-PHLPP2, or oe-SNAI2 + oe-PHLPP2. C p-Akt level in the presence of oe-NC, oe-SNAI2, oe-PHLPP2, or oe-SNAI2 + oe-PHLPP2 in nude mice xenografted with tumor as determined by Western blot assay. *p < 0.05 vs. nude mice xenografted with tumor injected with GSCs expressing oe-NC, si-NC, oe-SNAI2, or oe-PHLPP2. Each cell experiment was repeated three times independently. n = 10.
Fig 4: Molecular mechanism regarding the role of SNAI2 in GSCs via the Akt pathway by regulating PHLPP2 in GSC proliferation.SNAI2 downregulates PHLPP2 to activate the Akt pathway, thereby promoting the proliferation of GSCs.
Fig 5: GALNT6 promotes EMT in lung adenocarcinoma cells.A549, H1299, SPCA-1, and PC9 cells were transduced with control lentivirus (NC) or lentivirus for GALNT6 over-expression (G6-OE) or silencing (shNC, shG6-1/2), respectively. GALNT6, E-cadherin, N-cadherin and Slug expression in individual groups of cells were examined by immunofluorescent confocal microscopy and Western blot. a, c Immunofluorescence analysis. b, d Western blot analysis. Data are representative images or present as the mean ± SD of each group from three independent experiments. **p < 0.01; ***p < 0.001.
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