Abstract
Studies have confirmed the relationship between dysregulated long noncoding RNAs and melanoma pathogenesis. However, the regulatory functions of long intergenic non-protein coding RNA 1291 (LINC01291) in melanoma remain unknown. Therefore, we evaluated LINC01291 expression in melanoma and explored its roles in regulating tumor behaviors. Further, the molecular events via which LINC01291 affects melanoma cells were investigated. LINC01291 expression in melanoma cells was analyzed using The Cancer Genome Atlas database and quantitative real-time polymerase chain reaction. Functional assays, including the Cell Counting Kit-8 assay, colony formation assay, flow cytometry, cell migration and invasion assays, and tumor xenograft models, were used to examine LINC01291's role in melanoma cells. Additionally, bioinformatics analysis, RNA immunoprecipitation, luciferase reporter assay, and western blotting were conducted to determine the tumor-promoting mechanism of LINC01291. LINC01291 was upregulated in melanoma tissues and cell lines. Following LINC01291 knockdown, cell proliferation, colony formation, migration, and invasion were diminished, whereas apoptosis was enhanced and the cell cycle was arrested at G0/G1. In addition, loss of LINC01291 decreased the chemoresistance of melanoma cells to cisplatin. Furthermore, LINC01291 interference inhibited melanoma tumor growth in vivo. Mechanistically, LINC01291 functions as a competing endogenous RNA by sponging microRNA-625-5p (miR-625-5p) in melanoma cells and maintaining insulin-like growth factor 1 receptor (IGF-1R) expression. Rescue experiments revealed that the roles induced by LINC01291 depletion in melanoma cells could be reversed by suppressing miR-625-5p or overexpressing IGF-1R. Our study identified the LINC01291/miR-625-5p/IGF-1R competing endogenous RNA pathway in melanoma cells, which may represent a novel diagnostic biomarker and an effective therapeutic target for melanoma.