Fig. 4
From: BOK promotes chemical-induced hepatocarcinogenesis in mice
Loss of BOK affects cellular proliferation. a Immunohistochemistry showing Ki-67 staining in HCC tumors from WT and Bok-/- animals. b Quantification of Ki-67 positive cells in HCC tumors from WT and Bok-/- mice. Values represent the mean ± SD (n = 3 mice per group). c Growth curves and colony formation assay of IHH subclones with CRISPR/Cas9-mediated gene disruption of BOK. d Growth curves and colony formation assay of SV40 MEF derived from three different WT and Bok-/- embryos, each. Stable re-expression of BOK in Bok-/- SV40 MEF rescues the growth defect. e Stable re-expression of a BOK mutant, BOK(AAA), in which the predicted NES sequence within the BH3 domain has been mutated (L72A,R73A,L74A), fails to rescue the growth defect in Bok-/- SV40 MEF. Values represent the mean ± SD (n = 3). f BOK(AAA) accumulates in the cytoplasm compared to wildtype BOK. T total, C cytoplasmic fraction, N nuclear fraction. *p < 0.05, **p < 0.01, ***p < 0.005, ****p < 0.001
