Figure 1: BAP1 is a candidate DUB that maintains KLF5 protein stability.
From: BAP1 promotes breast cancer cell proliferation and metastasis by deubiquitinating KLF5
(a) Diagram of the screening procedure used to identify KLF5 DUBs. Eighty-seven siRNA pools were transfected into HeLa cells individually. Endogenous KLF5 protein levels were examined by WB after 48 h. (b) Validation of the five candidate KLF5 DUBs in HeLa cells. p27 is inhibited by KLF5. The siRNAs were transfected into HeLa cells, respectively, and endogenous KLF5 protein levels were measured by WB after 48 h. (c) BAP1 knockdown decreased KLF5 and FGF-BP, but increased p27 protein levels in various breast epithelial cell lines. MCF10A, HCC1806 and HCC1937 cells were transfected with control or two independent BAP1 siRNAs for 48 h. Luciferase (Luc) siRNA was used as the negative control. KLF5 siRNA was used as the positive control. The endogenous KLF5, FGF-BP and p27 protein levels were measured by WB. (d) BAP1 stable knockdown by shRNA#6 induced KLF5, FGF-BP and p27 protein expression changes were rescued by transient overexpression of BAP1, but not BAP1-C91S in HCC1806 and HCC1937 cells. For more data see Supplementary Fig. 10.
