Long non-coding RNAs (LncRNAs) have gained widespread interest and attention as vital regulators in cancer occurrence and development. Nonetheless, the functions and mechanisms of lncRNAs involved in nasopharyngeal carcinoma (NPC) are largely unknown. By analysing the data from GSE61218, we identified a novel lncRNA LINC01515 which is altered in NPC. A series of experiments were performed to examine the exact roles of LINC01515 as well as the molecular mechanisms by which LINC01515 acted in NPC. LINC01515 expression was increased in NPC and that high LINC01515 expression was associated with a worse prognosis. Functionally, depletion of LINC01515 resulted in an inhibition of cell proliferation, migration and invasion, while apoptosis was promoted. Mechanistically, LINC01515 facilitated cell division cycle associated 5 (CDCA5) expression via serving as a sponge for miR-325. And more notably, miR-325 suppressed NPC progression in vitro by targeting CDCA5. Furthermore, the anti-tumor property induced by LINC01515 knockdown was partially reversed due to the overexpression of CDCA5. Taken together, LINC01515 exerted the carcinogenic effect in NPC through regulating miR-325/CDCA5 pathway. Our findings shed light on the possibility of exploiting LINC01515 as a prognostic biomarker or therapeutic target in NPC.

长链非编码 RNA (LncRNAs) 作为癌症发生和发展的重要调节因子已引起广泛的兴趣和关注。尽管如此，涉及鼻咽癌（NPC）的lncRNA的功能和机制在很大程度上是未知的。通过分析来自 GSE61218 的数据，我们鉴定了一种在 NPC 中发生改变的新型 lncRNA LINC01515。进行了一系列实验以检查 LINC01515 的确切作用以及 LINC01515 在 NPC 中起作用的分子机制。LINC01515 在 NPC 中的表达增加，并且高 LINC01515 表达与较差的预后相关。在功能上，LINC01515 的消耗导致细胞增殖、迁移和侵袭的抑制，同时促进细胞凋亡。从机制上讲，LINC01515 通过充当 miR-325 的海绵促进细胞分裂周期相关 5 (CDCA5) 的表达。更值得注意的是，miR-325 通过靶向 CDCA5 抑制了体外 NPC 的进展。此外，由于CDCA5的过度表达，LINC01515敲低诱导的抗肿瘤特性被部分逆转。总之，LINC01515通过调节miR-325/CDCA5通路在NPC中发挥致癌作用。我们的研究结果阐明了利用 LINC01515 作为 NPC 预后生物标志物或治疗靶点的可能性。LINC01515通过调节miR-325/CDCA5通路在NPC中发挥致癌作用。我们的研究结果阐明了利用 LINC01515 作为 NPC 预后生物标志物或治疗靶点的可能性。LINC01515通过调节miR-325/CDCA5通路在NPC中发挥致癌作用。我们的研究结果阐明了利用 LINC01515 作为 NPC 预后生物标志物或治疗靶点的可能性。