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Objective   The current study investigated the effect of c-Jun NH2-terminal kinase (JNK) expression on the growth of transplanted breast cancer tumors in mice.Methods   A breast cancer transplantation model was established in BALB/c mice, which were then treated with SP600125 (30 mg/kg) for 24 days. After sacrificing the mice, the inhibitory effects of SP600125 on breast cancer growth were calculated by weighing tumors. Moreover, vascular endothelial growth factor (VEGF) expression and the tumor microvascular density (MVD) were evaluated via immunohistochemistry. Cell apoptosis was also examined using a TUNEL kit.Results   Compared with the findings in the control group, SP600125 treatment (30 mg/kg) obviously suppressed tumor growth during the 15-day observation period. SP600125 treatment markedly inhibited JNK mRNA expression. Furthermore, VEGF protein expression (50% vs. 100%) and MVD (18.27 ± 1.70 vs. 23.17 ± 4.02) were also significantly decreased by SP600125 treatment, whereas the apoptosis index was significantly higher in the treatment group (10.23 ± 1.97% vs. 4.53 ± 1.40%).Conclusion   Inhibition of JNK signaling can significantly suppress the growth of transplanted breast tumors in mice.

c-Jun NH2-terminal kinase suppression significantly inhibits the growth of transplanted breast tumors in mice