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. 2016 Feb 24;7(13):16311–16324. doi: 10.18632/oncotarget.7684

Figure 3. Low level of DIM activates β-catenin signaling to promote gastric cancer progression.

Figure 3

A. Real-time RT-PCR for the expression of WNT2, WNT3, WNT3a, WNT4, WNT5a, WNT6, WNT7b, WNT10b, and WNT11 genes in HGC-27 cells treated with 0, 1, and 10 μM DIM for 48 h. (n = 3, P < 0.05). B. Western blotting assays for β-catenin expression in HGC-27 cells treated with 0, 1, and 10 μM DIM for 48 h. C. HGC-27 cells were treated with 0, 1, and 10 μM DIM for 48 h. The nuclear translocation of β-catenin was determined by using immunofluorescence staining. Original magnification, 200Χ. D. Western blotting assays for the expression of SALL4, CD44, Oct4, Nanog, Sox2, Cyclin-D3, and PCNA proteins in HGC-27 cells treated with 1 μM DIM in the presence or absence of ICG001 (10 μM/ml) for 48 h. E. Representative images of cell colonies in HGC-27 cells treated with 1 μM DIM in the presence or absence of ICG001 (10 μM/ml). A. HGC-27 were treated with 1 μM DIM and 10 μM ICG001 for 7 days. B. HGC-27 cells were treated with 1 μM DIM and 10 μM ICG001 for 48 h, and then collected for colony formation assay for 7 days. F. Adipogenic differentiation of HGC-27 cells treated with 1 μM DIM in the presence or absence of ICG001 (10 μM/ml) for 48 h. Original magnification, 200Χ.