Artesunate attenuates the autophagy and apoptosis of choroidal melanoma via inhibiting TNFRSF19 through AKT/mTOR signaling pathway

Materials and methods: Databases including UALCAN, TIMER v2.0, and CCLE were used to examine the function of TNFRSF19 in Choroidal melanoma patients. Quantitative real-time polymerase chain reaction (qPCR) was employed to detect mRNA expression of TNFRSF19. With Western blot, the protein levels of the AKT/mTOR pathway, autophagy proteins (BECLIN1, ATG5, P62, and LC3II/LC3I), and apoptosis proteins (CASPASE3, Bax, and BCL2) were ascertained. The clonogenic assay, transwell assay, and other experiments were used to examine the proliferative and migratory capacities of choroidal melanoma. The autophagy protein p62 was tested via immunofluorescence labeling (IF). The TUNEL assay was used to measure apoptosis. A subcutaneous choroidal melanoma-transplanted human choroidal melanoma tumor model and lung metastasis model in nude mice was applied to test the effects of artesunate and TNFRSF19 in vivo. TNFRSF19 and Ki67 levels were examined using immunohistochemistry. Results: Our results demonstrated that TNFRSF19 enhanced growth and migration while inhabiting the autophagy and apoptosis in choroidal melanoma through activating AKT/mTOR signaling pathway. Artesunate reduced the expression of TNFRSF19 to prevent tumor growth of choroidal melanoma.