Long Non-Coding RNA-CASC15 Promotes Cell Proliferation, Migration, and Invasion by Activating Wnt/β-Catenin Signaling Pathway in Melanoma

Background: Melanoma is one of the most aggressive and high mortality skin cancers in the world. Long non-coding RNA-CASC15, as a carcinogen, plays an important role in a variety of tumorigenesis; however, the role and underlying mechanism of CASC15 in melanoma remain unclear. Methods: Quantitative real-time polymerase chain reaction was applied to explore CASC15 and beta-catenin expression in melanoma tissues and cells. Western blotting was carried out to investigate beta-catenin, glycogen synthase kinase-3 beta, Survivin, Bax, Bcl-2, and epithelial-mesenchymal transition (EMT)-related protein expression level. Cell proliferation, apoptosis, migration, and invasion were observed by colony formation assay, flow cytometry, and transwell migration and invasion assays, respectively. The activity of Wnt/beta-catenin signaling pathway was measured by Topflash luciferase reporter assay. Results: The expression of CASC15 and beta-catenin was upregulated in melanoma tissues and cells. Knockdown of CASC15 suppressed Wnt/beta-catenin signaling pathway and inhibited beta-catenin expression. Furthermore, inhibition of CASC15 decreased proliferation and increased apoptosis of melanoma cells by downregulating Survivin and Bcl-2 and upregulating Bax in A375 and SK-MEL-28 cells. Silencing of CASC15 inhibited migration and invasion of melanoma cells by repressing EMT process. Conclusion: Our study demonstrated that CASC15 promoted the proliferation, migration, and invasion of melanoma cells via activating Wnt/beta-catenin signaling pathway, implying that CASC15 might be a potential therapeutic target and prognostic biomarker for melanoma.