Melanoma is one of the most immunologic malignancies based on its higher prevalence in immune-compromised patients, the evidence of brisk lymphocytic infiltrates in both primary tumors and metastases, the documented recognition of melanoma antigens by tumor-infiltrating T lymphocytes and, most important, evidence that melanoma responds to immunotherapy.,The use of immunotherapy in the treatment of metastatic melanoma is a relatively late discovery for this malignancy.,Recent studies have shown a significantly higher success rate with combination of immunotherapy and chemotherapy, radiotherapy, or targeted molecular therapy.,Immunotherapy is associated to a panel of dysimmune toxicities called immune-related adverse events that can affect one or more organs and may limit its use.,Future directions in the treatment of metastatic melanoma include immunotherapy with anti-PD1 antibodies or targeted therapy with BRAF and MEK inhibitors.
As a member of the microRNA (miR)-17-92 cluster, miR-20a has been indicated to be involved in the regulation of the proliferation and invasion of various cancer cells.,Previous studies have observed elevated plasma levels of miR-20a in patients with uveal melanoma (UM), compared with normal controls.,In the present study, the potential function of miR-20a in UM was investigated.,Reverse transcription-quantitative polymerase chain reaction analysis was performed to detect the expression levels of miR-20a in UM cells and tissues.,The functions of miR-20a on cell proliferation, migration and invasion were determined in vitro using 3-(4,5-dimethyl-thiazol-2-yl)-2,5-diphenyltetrazolium bromide and Transwell assays, respectively.,The expression levels of miR-20a were significantly increased in the UM cells and tissues (P<0.05).,Subsequently, miR-20a mimics were transfected into UM cells, which led to increases in cell growth, migration and invasion activities.,By contrast, miR-20a inhibition markedly suppressed the viability and motility of UM cells in vitro.,These data provided convincing evidence that miR-20a may function as an oncogenic miRNA, and may be involved in promoting cell growth and motility in the molecular etiology of UM, suggesting its potential as a candidate therapeutic target for the treatment of patients with UM.