531 Opsin 3 promotes invasion of melanoma cells in an artificial melanoma model

Abstract

Opsin is family of G protein-coupled receptors (GPCRs) and serve a variety of nonvisual functions. Our recent study found that high opsin 3 expression is significantly associated with ALM and metastatic phenotype. The artificial melanoma model can simulate the physiological state of the skin and avoid harm to animals which is a good model for studying the pathogenesis of melanoma invasion. Whether opsin 3 can promote the invasion of melanoma cells and replicate clinically observed phenomena in artificial melanoma models is not yet clear. Objective: To investigate whether Opsin 3 promote invasion of melanoma cells in artificial melanoma model. Method: Used the GFP-opsin3 plasmid to constructed an MV3 melanoma cell line stably overexpressed opsin 3 and vector group as a control. Transfection efficiency observed by fluorescence microscope and opsin3 stably overexpression in MV3 detected by western blot. Compared the invasion and migration ability of MV3 cells in the with or without overexpression opsin 3 through Transwell. Overexpression GFP-opsin3 MV3 cells and control cells were seeded onto the DED and maintained at the air-liquid interface after submerged culture about8,12,15 days. Then HE was used to detect the distribution of MV3 cells on the reconstructed melanoma tissue in different group. Result: Opsin 3 was stably overexpressed in MV3 cells. Transwell showed that MV3 cells in the opsin 3 overexpression group had stronger invasion and migration capabilities. The artificial melanoma model was successfully constructed, and the HE results showed that MV3 cells disturbed at the surface of DED and gathered circularly at lumina of the cutaneous appendages.MV3 cell which are with or without overexpression of opsin 3 could invade down the porosity on the surface of the DED, but more obvious performance in overexpression opsin 3 group. Conclusion: Opsin 3 could promote invasion of MV3 melanoma cells in an artificial melanoma model.