Abstract
Uveal melanoma (UM) is the most common ocular malignancy and has no effective clinical treatment. Therefore, novel drugs to suppress UM tumor progression are urgently required. The present study aimed to clarify the underlying mechanism of the inhibitory effects of artesunate on UM. By using plasmid transfection and detecting apoptotic level, the present study identified artesunate as a potential candidate for UM treatment. Compared with those in the vehicle (DMSO)-treated control cells, artesunate enhanced the apoptotic rate and increased lactate dehydrogenase release, reactive oxygen species and IL1b and IL18 levels in C918 cells. Overexpression of yes-associated protein (YAP) or metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in C918 cells reversed the effects of artesunate and reduced the apoptotic rate compared with those observed in cells transfected with the negative control plasmid. Notably, verteporfin enhanced the effects of artesunate on C918 cells by increasing the apoptotic rate, indicating that combined therapy was more effective compared with treatment with artesunate alone. In conclusion, the results of the present study demonstrated that artesunate elevated the apoptotic rate and suppressed C918 cell viability by regulating the MALAT1/YAP signaling pathway, and these effects were enhanced by supplementation with verteporfin. These results suggested that artesunate may exert an inhibitory effect on C918 cells and that the MALAT1/YAP signaling may serve important role in mediating these effects, providing evidence of its potential for treating UM in the clinic.