Egr-3 contributes to B16-melanoma tumor progression in mice. (A) B16-F10 melanoma cells and Lewis lung carcinoma (LLC) cells were injected subcutaneously into C57/BL6j mice. After 14 days, solid tumor xenografts (1 mm³) were removed, cryosectioned, and immunostained with anti–Egr-3 antibody (left) or anti–PECAM-1 antibody (middle). Merged images with DAPI are shown on the right. White bar indicates 50 μm. (B) Gross pathology of B16-F10 melanoma from Ad-miControl– or Ad-miEgr-3–injected groups immediately after resection (left). Graph shows tumor volume in Ad-miControl–injected (●) or Ad-miEgr-3–injected (○) mice. Arrow indicates the day of adenovirus injection. Data represent mean ± SEM n = 6. *P < .01 compared with Ad-control and Ad-miEgr3. (C) Representative cryosections of B16-F10 melanoma stained with anti–PECAM-1 antibody (left). Vascular density was calculated on the basis of the number of PECAM-1–positive cells. The mean ± SD were derived from 3 optical images of 3 separate xenografts in each condition (right). *P < .001 compared with Ad-miControl. (D) Representative cryosections of B16-F10 melanoma stained with anti-CD45 antibody. Inflammatory leukocytes infiltration levels were calculated on the basis of numbers of CD45-positive cells per optical field (×200, Leica [DMLB]). The mean ± SD were derived from 6 optical images of 6 independent xenografts in each condition (bottom). *P < .001 compared with Ad-miControl.