Functional MoS2 nanosheets inhibit melanogenesis to enhance UVB/X-ray induced damage

Abstract

The overproduction of melanin not only causes a series of hyperpigmentation dermatosis but also protects melanoma from radiation. Many studies have shown that scavenging ROS can inhibit melanogenesis by inactivating the p38 mitogen-activated protein kinase (MAPK) pathway. Molybdenum disulfide (MoS2) has been reported to scavenge ROS in cells but has not been implicated in the regulation of melanin. Here, we use tryptophan (Trp), which has a nonpolar indole ring serving as an effective exfoliating and stabilizing agent, to produce highly dispersed MoS2 nanosheets in water. LA-PEG was further functionalized to enhance the stability under physiological conditions. MoS2-Trp-PEG showed no toxicity on murine melanoma B16F10 cells and could scavenge ROS, inactivate the p38 MAPK pathway and downregulate the expression of MITF, resulting in inhibition of melanogenesis. Besides, MoS2-Trp-PEG could enhance UVB/X-ray-induced B16F10 cell damage in vivo and melanoma inhibition in vitro, which were possibly related to improving the radiosensitivity of melanoma by inhibiting melanogenesis. These findings may provide a potential strategy for the treatment of hyperpigmentation dermatosis; MoS2-Trp-PEG, and similar transition metal dichalcogenide materials with the activity of scavenging ROS, might be applied to increase the radiosensitivity of melanoma by inhibiting melanogenesis.