Abstract
Neuroindole melatonin, a hormone synthesized during the night mainly—but notexclusively—by the pineal gland of all vertebrates, functions as an adapting signal to the light-darkcycle. Its antioxidant, neuroprotective, anti-inflammatory, and antitumor properties are all well-knownand widely reported. Melanoma is one of the most common carcinomas among developed countriesand a type of tumor particularly difficult to fight back in medium/advanced stages. In contrast toother types of cancer, influence of melatonin on melanoma has been scarcely investigated. Thus, wehave chosen the murine melanoma model B16-F10 cell line to study antiproliferative and antitumoralactions of melatonin. For this purpose, we combined both, cell culture and in vivo models. Melatoninreduced either, growth rate or migration of B16-F10 cells. Furthermore, melanin synthesis was alteredby melatonin, promoting its synthesis. Melatonin also induced a G2/M cell cycle arrest and alteredthe cytoskeletal organization. To corroborate these results, we tested the effect of melatonin in thein vivo model of B16-F10 cell injection in the tail vein, which causes numerous lung metastases.Two different strategies of melatonin administration were used, namely, in drinking water, or dailyintraperitoneal injection. However, contrary to what occurred in cell culture, no differences wereobserved between control and melatonin treated groups. Results obtained led us to conclude thatmelatonin exerts an antiproliferative and anti-migrating effect on this melanoma model by interferingwith the cytoskeleton organization, but this pharmacological effect cannot be translated in vivo asthe indole did not prevent metastasis in the murine model, suggesting that further insights into theeffects of the indole in melanoma cells should be approached to understand this apparent paradox