ADAM10 promotes uveal melanoma development by regulating the wnt/β-catenin pathway

Uveal melanoma (UVM) seriously affects people's health and quality of life. Here, the mechanism of a disintegrin and metallopeptidase domain 10 (ADAM10) was elucidated in UVM.

The clinical prognosis and potential biological function of ADAM10 gene in UVM patients were assessed using a series of bioinformatics methods. RT-qPCR and Western blot assay were employed to detect genes expression. Cell apoptosis and viability were examined by flow cytometry, clone formation and CCK-8 assays. The migrated and invasive abilities were analyzed by wound healing and transwell assays. Tumor growth was performed in Xenograft mouse model.

We found that ADAM10 expression was significantly associated with poor prognosis of UVM patients, and its prognostic significance for UVM patients was determined by distinct clinical characteristics. In vitro, ADAM10 expression was upregulated in MUM-2B and C918 UVM cell lines. More importantly, ADAM10 downregulation discouraged cell viability, metastasis but triggered apoptosis of UVM cells. Moreover, ADAM10 upregulation can promote the tumor growth of UVM in vivo. Mechanically, ADAM10 downregulation blocked the Wnt/β-catenin pathway in UVM.

Downregulation of ADAM10 discourages the malignant behaviors of UVM through inhibiting the Wnt/β-catenin pathway.