LncRNA GAS5 is a critical regulator of metastasis phenotype of melanoma cells and inhibits tumor growth in vivo.

The present study intended to demonstrate the effects of long noncoding RNA growth arrest-specific transcript 5 (GAS5) on the migration and invasion of melanoma cells. We first detected the expression of GAS5 among four kinds of melanoma cell lines, followed by constructing GAS5-knocked down and overexpressed stable cells. Next, we evaluated the effects of GAS5 on cell migration and invasion using wound healing and gelatin zymography assays. Finally, melanoma cells with different GAS5 expression were injected into nude mice, and the tumor volumes were recorded and tumor tissues were analyzed after sacrificing the mice. This study systematically examined the function of GAS5 in mediating melanoma metastasis and revealed that GAS5 plays an anticancer role in melanoma via regulating gelatinase A and B, both in vitro and in vivo.

Lentiviral-mediated overexpression of long non-coding RNA GAS5 reduces invasion by mediating MMP2 expression and activity in human melanoma cells.

The present study evaluated the effects of long non-coding RNA GAS5 on the migration and invasion of melanoma cells. Using the SK-Mel­110 melanoma cell line, we stably expressed GAS5, visualized the distribution of GAS5 by RNA fluorescence in situ hybridization (FISH) and examined changes in cell migration and invasion with Transwell assays. In GAS5 overexpressed SK-Mel­110 cells, migrated and invaded cells decreased by 65.3 and 55.6%, respectively. Moreover, the MMP2 protein level, and its activity was downregulated by 67.9 and 15.8%, respectively. Overexpressing lncRNA GAS5 inhibited the migration and invasion ability of melanoma SK-Mel­110 cells, partially by decreasing the MMP2 expression and its activity. This study is the first to reveal a potential relationship between lncRNA GAS5 and the migration and invasion of melanoma.