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https://www.selleckchem.com/products/ficz.html ients and treatment strategies. The expression of LINC01198 is upregulated in the case of CRC, which promotes proliferation and inhibits apoptosis of CRC cells by regulating the Notch signaling pathway. Our findings provide a novel biomarker for the diagnosis and treatment of HCC patients and treatment strategies. Melanoma is one of the most malignant types of skin tumors and accounts for the majority of skin cancer-related deaths. LINC00662 is a tumor promoter in multiple types of cancer, but the role of LINC00662 in melanoma has not been fully elucidated. The expression levels of LINC00662, miR-890, and ELK3 were detected by Real Time-quantitative Polymerase Chain Reaction (RT-qPCR). MTT assay was performed to measure the cell proliferation ability in A375 and SK-MEL-1 cells. Cell migration and invasion abilities were measured by wound healing assay and transwell assay, respectively. Besides, Luciferase reporter assay was employed to examine the interaction between miR-890 and LINC00662 or ELK3. In the present study, it was demonstrated that melanoma patients with high expression levels of LINC00662 had a shorter survival time than those with low expression levels of LINC00662. LINC00662 exhibited higher expression levels in melanoma tissues and cell lines. Additionally, suppression of LINC00662 impaired cell proliferation, migration, and invasion. Furthermore, animal experiments demonstrated that LINC00662 facilitated tumor growth in vivo. LINC00662 was confirmed to bind with miR-890, and ELK3 was identified as a downstream target gene of miR-890. Furthermore, miR-890 was found to negatively regulate ELK3 expression. Through rescue assays, overexpression of ELK3 reversed the inhibitive effects of LINC00662 knockdown or miR-890 mimics on the cell proliferative, migratory, and invasive abilities. Our results demonstrated that LINC00662 facilitated the occurrence and development of melanoma by sponging miR-890 to upregu

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