The effects of blue light on B16 melanoma cells and on the metastasis of these cells to the lungs were investigated in mice. The exposure of B16 melanoma cells to blue light in two 20-min sessions resulted in marked suppression of cell growth measured at 7 days after exposure. When these cells were harvested, re-inoculated into medium and incubated for a further 7 days, their growth activity returned to almost the same level as that of cultured cells from the non-exposure control group. The melanoma cells harvested after 7 days of incubation were injected intravenously into mice. In the non-exposure group, black nodules developed on the lung surface and the nodules increased in size over time. In the blue-light-exposure group, the development of such black nodules on the lung surface was delayed, and the nodules were smaller. Histopathological examination revealed that blue light suppressed the growth of metastatic tumor cells, and no increase in the number of melanin-containing cells or atypical cells was induced in the metastatic lesions. These results suggest that blue light suppresses the metastasis of B16 melanoma cells.

A number of polysaccharides exhibit pharmacological activities. Polysaccharides derived from Inonotus obliquus (PLIO) appear to have various potential pharmacological properties, including anti‑tumor activity. However, the molecular mechanisms underlying these properties remain to be elucidated. The present study investigated the anti‑metastatic potential of PLIO and the underlying signaling pathways in B16‑F10 murine melanoma cells using the MTT colorimetric assay, in vitro migration and invasion assays, and flow cytometric and western blot analyses. PLIO inhibited the invasion of B16‑F10 cells and suppressed the expression of matrix metalloproteinases. PLIO treatment inhibited nuclear factor‑κB (NF‑κB) nuclear translocation in B16‑F10 cells. In addition, PLIO treatment inhibited the phosphorylation of c-Jun N‑terminal kinases and AKT. These results suggest that PLIO may suppress the invasion of highly metastatic melanoma cells via inhibition of the AKT/NF-κB signaling pathways.

Vitamin C has been used in complementary and alternative medicine for cancers regardless of its ineffectiveness in clinical trials and the paradoxical effects antioxidants have on cancer. Vitamin C was found to induce cytotoxicity against cancers. However, the mechanisms of action have not been fully elucidated, and the effects of vitamin C on human malignant melanoma have not been examined. This study revealed that vitamin C at millimolar concentrations significantly reduced the cell viability as well as invasiveness, and induced apoptosis in human malignant melanoma cells. Vitamin C displayed stronger cytotoxicity against the Vemurafenib-resistance cell line A2058 compared with SK-MEL-28. In contrast, vitamin C at micromolar concentrations promoted cell growth, migration and cell cycle progression, and protected against mitochondrial stress. Vemurafenib paradoxically activated the RAS-RAF-MEK-ERK signaling pathway in the Vemurafenib-resistant A2058, however, vitamin C abolished the activations. Vitamin C displayed synergistic cytotoxicity with Vemurafenib against the Vemurafenib-resistant A2058. In vivo assay suggested that lower dosage (equivalent to 0.5g/70kg) of vitamin C administered orally increased the melanoma growth. Therefore, vitamin C may exert pro- or anti-melanoma effect depending on concentration. The combination of vitamin C at high dosage and Vemurafenib is promising in overcoming the action of drug resistance. This article is protected by copyright. All rights reserved.