Objective This study aimed to investigate the relationship between traumatic stress and tumor growth, proliferation, and metastasis.Methods A scalding method was used as an injurious factor to induce traumatic stress in Wistar rats. The rats were randomly divided into three groups—the control group, mild-scald group, and severe-scald group, with 14 rats in each group. Wistar rats were used to subculture the Walker-256 cell line for the generation of tumor ascites. Tumor cells from the ascites were cultured and used to establish a rat subcutaneous xenograft model. After 7 days, the mild-b group and the severe-b group were subjected bs to 10％ and 15％ of their backs, respectively. Blood was taken from the tail vein of rats at different times to detect changes in blood cortisol, IL-1β, and TNF-α levels. Pathological specimens were collected 14 days later, and immunohistochemistry was performed to examine vascular endothelial growth factor (VEGF), proliferating cell nuclear antigen (PCNA), E-cadherin, and vimentin. Results Cortisol, IL-1β and TNF-α levels were significantly higher in the scalding groups than in the control group. Tumor examination was performed after 14 days. The changes in tumor size showed that the tumor volume in the control group (0.593 ± 0.195 cm3) and the mild-scald group (0.782 ± 0.344 cm3) were not significantly different. However, the tumor volume was significantly larger in the severe-b group (1.806 ± 0.838 cm3) than in the control and the mild-b groups(P < 0.05). Tumor tissue immunohistochemistry showed that the percentage of cells expressing PCNA in the control group, mild-scald group, and severe-scald group was 57.1％, 71.4％ and 85.7％, respectively, and the differences among the groups were statistically significant. The number of VEGF-positive cells in the mild- and severe-scald groups was significantly higher than those of the control group (P < 0.05). The number of E-cadherin-positive cells in the tumor tissues was significantly lower in the severe-scald group than that in the control and mild-scald groups. Vimentin showed the opposite trend in the tumor tissue, and the differences were statistically significant (P < 0.05). Conclusion Different degrees of a traumatic response in tissues caused by scalding can cause a corresponding stress response in the body. The release of inflammatory mediators; increase in VEGF, PCNA and vimentin in the tumor tissue; and decrease in E-cadherin lead to a change in tumor tissue growth and metastasis. Traumatic stress is associated with tumor growth, proliferation, and metastasis.