Fig. 5
From: The FBXW7-binding sites on FAM83D are potential targets for cancer therapy
FBXW7 deficiency mediates the oncogenic roles of FAM83D. a-d, FBXW7 expression plasmid or empty vector was introduced into FAM83D-overexpressed MCF7 cells. The effects of FBXW7 re-expression on FAM83D-induced cell proliferation were detected by clonogenic assay (a) and CCK8 assay (b). The effects of FBXW7 re-expression on FAM83D-induced cell invasiveness and migration were determined by wound-healing assay (c) and Matrigel coated or uncoated Transwell assay (d). e-f, FBXW7-specific shRNA (shFBXW7 56 and shFBXW7 58) or control shRNA was introduced into FAM83D-silenced BT-549 cells. The effects of FBXW7 depletion on FAM83D loss-induced cell proliferation inhibition were examined by clonogenic assay (e) and CCK8 assay (f). Graphs in a, c, d and e presented quantification analyses. Data were presented as mean ± SD. ns: not significant. *: p < 0.05, **: p < 0.01, ***: p < 0.001 based on the Student’s t-test