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. Author manuscript; available in PMC: 2017 Oct 15.
Published in final edited form as: Cancer Res. 2017 Feb 16;77(8):1983–1996. doi: 10.1158/0008-5472.CAN-16-2246

Figure 5. EBP1 P48 mediates the tumor suppressing function of FBXW7.

Figure 5

A and B. MTT (A) and colony formation (B) analyzes were used to detect the influence of EBP1 P48 knockdown on FBXW7 loss-induced cell proliferation of HCT116 cells. The graph shows quantitative analysis. C and D. The influence of EBP1 P48 knockdown on FBXW7 loss-induced migration and invasion ability of HCT116 cells was determined by wound healing (C), uncoated or Matrigel-coated transwell assay (D). The graphs show quantitative analysis. E. The total numbers of nude mice with distant metastasis at 40–50 days after injection of HCT116 FBXW7+/+, HCT116 FBXW7−/− or HCT116 FBXW7−/− cells with silent EBP1 P48 into tail vein. F and G. The representative HE staining and numbers of metastatic foci per section in lung (F) and liver (G) of individual mouse with injection of indicated cells. The scale bars in (C) represents 500μm, in (D, F, G) represent 50μm and in the inserts of (F, G) represent 20μm. H and I. Anti-human GAPDH antibody which does not react with mouse GAPDH was used to distinguish the colonized cell population between human and mouse by IHC. The results from (A–E) are repeated at least three times. ** P<0.01 based on Student t-test.