Figure 6.

Loss of Connexin37 decreases the growth of B16-F10 tumors and extends the survival of the tumor-bearing mice. B16-F10 cells were s.c. injected to generate tumors in WT and Cx37−/− mice. (A) The volume of the tumors growing in Cx37−/− mice until day 15 was significantly smaller than that of the tumors growing in WT animals. Data are mean ± SEM of WT mice (n = 11, black line) and Cx37−/− mice (n = 13, dotted red line). **** p< 0.0001 versus WT mice (areas under the tumor growth curve were compared by Student’s t-test). (B) In another set of mice, which were sacrificed 14 days after the cell injection, the hemoglobin content of the tumors grown in Cx37−/− mice was lower than that evaluated in the WT controls. (C) Immunostaining showed a similar distribution of NG2 over the VeCad positive vessels of the B16-F10 tumors which grew in WT and Cx37−/− mice. (D) Immunostaining of pimonidazole (green) revealed hypoxic areas in tumor regions containing VeCad-positive vessels (red). Quantitative analysis revealed that the surface of these hypoxic areas was comparable in the tumors grown in Cx37−/− and WT mice. Data are mean + SEM of 8–15 fields from 7 mice per group (Student’s t-test). Bars = 100 μm. (E) The survival of the Cx37−/− mice that carried a B16 tumor was significantly increased compared to that of the cognate WT animals. Data are mean ± SEM of 11 WT mice (black line) and 13 Cx37−/− mice (dotted red line). * p < 0.05 versus WT mice (log-rank Mantel-Cox test).