The mechanism of sodium butyrate on the growth of mouse B16 melanoma cells by inhibiting the differentiation of M2-type macrophages and down-regulating the expressions of VEGF and TGF-β.

Melanoma is a highly malignant cancer with a high differentiation potential and metastatic capacity. Sodium butyrate, known for its anti-cancer activity, is used in various types of solid tumors. This study aimed to investigate the effects of sodium butyrate on B16 melanoma cells using in vitro and in vivo mouse models. The study utilized MTT assay, flow cytometry, and immunoblot analysis. Mice were treated with normal saline (control) or 1 mM, 2 mM, 3 mM, or 5 mM sodium butyrate. Results showed that cell viabilities were significantly reduced in 2 mM, 3 mM, and 5 mM sodium butyrate groups after 24 to 48 hours (p < 0.01 for all). Moreover, sodium butyrate exhibited a tumor suppression effect that was time-dependent and lasted for 30 days (p < 0.01 for all). A significant tumor suppression effect was observed in the case of 5 mM sodium butyrate after 30 days (p < 0.001 for all). As compared to control (no sodium butyrate), tumor-associated macrophages were decreased in 2 mM, 3 mM, and 5 mM sodium butyrate groups (<0.01 for all). The maximum reduction was observed in 5 mM sodium butyrate groups. Sodium borate decreased the release of interleukin-10, vascular endothelial growth factor, transforming growth factor beta, and β-actin (<0.01 for all). A significant reduction was observed in the case of 5 mM concentration. Overall, these findings suggest that sodium butyrate is effective in the treatment of melanoma and may offer a promising new avenue for melanoma therapy.