Abstract
Melanoma is a skin cancer characterized by early metastasis and high mortality. Radiotherapy is a common treatment for melanoma in patients. Long noncoding RNAs play pivotal roles in regulating the radiosensitivity of many tumors, including melanomas. In this study, the role of LINC01224 in the radiosensitivity of melanoma cells was explored. The expression of LINC01224 in melanoma was examined by reverse transcription-quantitative polymerase chain reaction, and the results showed that LINC01224 was upregulated in melanoma tissues and cells. The effects of LINC01224 on cell proliferation and apoptosis in melanoma were assessed by 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide (MTT), colony formation, and flow cytometry assays. The effects of LINC01224 on the radiosensitivity of melanoma were analyzed by colony formation assay. The results implied that LINC01224 knockdown inhibited cell viability and proliferation but enhanced cell apoptosis and radiosensitivity. Luciferase reporter and RNA pull-down assays were performed to evaluate the relationships between LINC01224 and miR-193a-5p or miR-193a-5p and nuclear receptor subfamily 1 group D member 2 (NR1D2). We found that LINC01224 binds to miR-193a-5p, which directly targets NR1D2. In addition, we discovered that LINC01224 upregulated NR1D2 expression by sponging miR-193a-5p in melanoma cells. Overall, the data collected in this study suggest that LINC01224 exerts oncogenic effects in melanoma via the miR-193a-5p/NR1D2 axis.