Long noncoding RNAs (lncRNAs) play crucial roles in
melanoma initiation and development, serving as potential therapeutic targets and prognostic markers for
melanoma.
lncRNA survival-associated mitochondrial
melanoma-specific oncogenic
noncoding RNA (SAMMSON) is upregulated in many types of human
cancers. However, the functions of SAMMSON in
melanoma have not been fully elucidated. This study is aimed at investigating the expression and functions of SAMMSON in
melanoma development. Bioinformatics analysis was performed to determine the expression of SAMMSON and its correlation with the 10-year overall survival (OS) in
melanoma patients. Cell proliferation, migration, invasion, and
tumorigenesis were detected by MTT, colony formation, Transwell assays, and mouse xenograft model. The expression of cell cycle-related factors, epithelial-to-mesenchymal transition (EMT) makers, and
matrix metalloproteinases (
MMPs) was assessed by RT-qPCR and western blotting analysis. The results demonstrated that SAMMSON expression was upregulated in
melanoma tissues and cells, and lower SAMMSON expression was correlated with longer 10-year OS. SAMMSON knockdown decreased the proliferation, migration, and invasion of
melanoma cells by regulating the expression of proliferation-related genes, EMT factors, and
MMPs, respectively. Additionally,
Forkhead box protein A2 (FOXA2) was confirmed to be a target of SAMMSON, and the biological effects induced by FOXA2 overexpression were similar to those induced by SAMMSON silencing in
melanoma cells. Further studies showed that SAMMSON downregulated FOXA2 expression in
melanoma cells by modulating the EZH2/H3K27me3 axis. Taken together, our data indicate that SAMMSON plays an important role in
melanoma progression and can be a valuable
biomarker and therapeutic target in
melanoma.