BACKGROUND
Melanoma is one of the most aggressive types of
cancer and it has shown a remarkable surge in incidence during the last 50 years.
Melanoma has been projected to be continuously rising in the future.
Therapy for advanced-type
melanoma is still a challenge due to the low response rate and poor 10-year survival. Interestingly, several epidemiological and preclinical studies had reported that
vitamin D deficiency was associated with
disease progression in several
cancer types. In vivo and in vitro studies revealed anti-proliferative, anti-angiogenic, apoptosis, and differentiation induction effects of
calcitriol in various
cancers. However, information on the effects of
calcitriol (1,25(
OH)₂D₃) on
melanoma is still limited, and its mechanism remains unclear. MATERIAL AND METHODS In the present study, by utilizing B16-F10 cells, which is a
melanoma cell line, we explored the anti-proliferative effect of
calcitriol using cell viability assay, near-infrared imaging, expression of apoptosis-related genes using real-time polymerase chain reactions (PCR), and the expression of apoptosis
proteins levels using western blot. In addition, we also assessed
calcitriol uptake by B16-F10 cells using high-performance liquid chromatography (HPLC). RESULTS We found that
calcitriol inhibits
melanoma cell proliferation with an IC₅₀ of 93.88 ppm (0.24 μM), as shown by cell viability assay. Additionally, we showed that B16-F10 cells are capable of
calcitriol uptake, with a peak uptake time at 60 min after administration.
Calcitriol was also able to induce apoptosis-related
proteins such as
caspase-3,
caspase 8, and
caspase-9. These effects of
calcitriol reflect its potential utility as a potent adjuvant
therapy for
melanoma. CONCLUSIONS
Calcitriol inhibits cell proliferation and induces apoptosis in B16-F10 cells.