Boron's Role in B16-F10 Melanoma: Cytotoxic, Antioxidant, Apoptotic, and Anti-inflammatory Effects.

Malignant melanoma is a fatal cancer type with a high risk of metastasis. Despite traditional treatments, the survival time of patients is usually 3-9 months. Therefore, alternative treatment strategies are needed. This in vitro study aimed to examine the potential role of boric acid in melanoma treatment by evaluating its cytotoxic, oxidative stress-related, anti-inflammatory, and apoptotic effects on the B16-F10 mouse melanoma cell line. B16-F10 cells were treated with boron at concentrations ranging from 1-100 mM for 24-48 h. Quantitative assays (n = 6 biological replicates per group) showed that boron induced dose-dependent apoptosis and significantly reduced cell viability (IC₅₀ = 16 mM). Annexin-V protein levels increased by 2.1-fold (p < 0.001) at 16 mM, while Bcl-2 protein decreased by 40% (p = 0.037). Conversely, Bcl-2 mRNA expression declined at high doses, suggesting post-transcriptional regulation. Bax and p53 gene expressions increased by 1.35-fold and 7.7-fold, respectively (both p = 0.000). Oxidative stress markers showed a 1.8-fold increase in MDA (p < 0.01) and a 25% increase in GSH (p < 0.05), indicating a redox imbalance with partial compensatory antioxidant response. The results demonstrated that boron treatment induced dose-dependent apoptosis by reducing cell viability, compared to the untreated control cells. In the cells treated with boron, while Bcl-2 gene expression was decreased, the expression of Bax, p53 gene expressions and the level of annexin-V was increased. It was also seen that TNF-α and IL-6 mRNA expression levels and IL-1β and IL-10 levels were decreased in the cells treated with boron. Following boron treatment, an increase in CAT activity, as well as higher levels of GSH and MDA, was observed. These findings suggest that boron may exert anti-melanoma effects in vitro by promoting apoptosis, modulating redox and inflammatory pathways, creating oxidative stress, and decreasing TNF-α and IL-6 levels. However, further in vivo studies are required to validate its therapeutic potential, supporting its evaluation as a promising cancer treatment agent.