Fig. 1

Knockout of cyclin G2 in macrophages attenuates the tumor suppressive effects of IFN-γ. A CCNG2 mRNA expression in THP-1 cells treated with IFN-γ, LPS, IL-4 and IL-13 was detected RT–qPCR using β-actin as an internal control. Data are presented as the mean ± SD (Data of CCNG2 mRNA expression in THP-1 cells treated with IFN-γ representing 3 independent experiments). B Cyclin G2 protein levels in THP-1 cells treated with IFN-γ, IL-4 and IL-13 were evaluated by western blotting using β-tubulin as a loading control (representing 3 independent experiments). C Cyclin G2 protein levels in the human peripheral blood monocytes were determined by western blotting following IFN-γ, IL-4 and IL-13 treatment. β-tubulin was used as a loading control (representing 3 independent experiments). D After IFN-γ (100 ng/mL) treatment of BMDMs, the cyclin G2 protein expression was detected by western blotting. β-tubulin was used as a loading control (representing 3 independent experiments). E BMDMs were isolated from WT and Ccng2^−/− C57BL/6 mice and identified by western blotting. β-tubulin was used as a loading control. F LLC cells were mixed with BMDMs from WT and Ccng2^−/− C57BL/6 mice at a ratio of 5:1 and injected subcutaneously into C57BL/6 mice, which were then treated with IFN-γ at specific times. G–J Gross tumors (G), tumor growth curves (H), and tumor weights (I) and volumes (J) measured at the study endpoint. (n = 5). K Representative Ki-67 immunohistochemical staining of tumors from mice in the WT and Ccng2^−/− groups. 10× scale bar = 200 μm; 40× scale bar = 50 μm. (L) Graph showing the number of Ki-67-positive cells in each field (n = 5). The data in H, I, J, and L are presented as the mean ± SEM. Data presented in A, I, J, and L were analyzed with the unpaired Student’s t-test. Data in H were analyzed using two-way ANOVA. *p < 0.05; ***p < 0.001; ****p < 0.0001; ns, not significant