Increased expression of long noncoding RNA GAS6-AS2 promotes proliferation and inhibits apoptosis of melanoma cells via upregulating GAS6 expression.

Long noncoding RNAs (lncRNAs) are frequently aberrantly expressed and involved in many cancers, including melanoma. GAS6-AS2 was a recently identified cancer-related lncRNA. However, the expression, roles, and functional mechanisms of GAS6-AS2 in melanoma remain unknown. In this study, we found that lncRNA GAS6-AS2 is significantly elevated in melanoma tissues and cells. Elevated expression of GAS6-AS2 is positively correlated with advanced stages and poor prognosis in melanoma. Functional assays demonstrated that ectopic expression of GAS6-AS2 promotes proliferation and inhibits apoptosis of melanoma cells. In contrast, knockdown of GAS6-AS2 inhibits proliferation and promotes apoptosis of melanoma cells. Furthermore, in vivo functional assays showed that GAS6-AS2 promotes melanoma xenograft growth. Mechanistically, we found that GAS6-AS2 upregulates GAS6 expression, promotes GAS6 secretion, and activates AXL/AKT/ERK signals. The expression of GAS6 was positively correlated with that of GAS6-AS2 in melanoma tissues. In addition, deficiency of GAS6 reverses the biological roles of GAS6-AS2 overexpression in melanoma cell proliferation and apoptosis. Collectively, our data identified GAS6-AS2 as an oncogenic lncRNA in melanoma via activation of GAS6/AXL/AKT/ERK signals. Our data suggested that GAS6-AS2 may be a novel potential prognostic biomarker and therapeutic target for melanoma.