本研究的目的是探究马达蛋白超家族成员15（KIF15）在鼻咽癌（NPC）发生中的作用及其潜在机制。我们采用了多种实验方法，包括CCK-8实验、流式细胞仪、Transwell和划痕实验、Western blotting以及裸小鼠移植肿瘤，研究KIF15对NPC的影响。我们的研究结果表明，KIF15在NPC细胞的增殖、凋亡、迁移和侵袭中起着关键作用。此外，我们发现沉默KIF15可以抑制细胞增殖、迁移和侵袭，促进凋亡，KIF15对NPC细胞的生长影响通过PI3K/AKT和P53信号通路介导。此外，我们还证明KIF15促进鼻咽癌细胞在体内的生长。本研究揭示了KIF15在NPC中的重要性，通过调节与AKT相关的信号通路，KIF15沉默抑制NPC细胞的生长。这些发现表明KIF15是预防和治疗NPC的有希望的治疗靶点。

The aim of this study was to investigate the role of kinesin superfamily member 15 (KIF15) in nasopharyngeal carcinogenesis (NPC) and explore its underlying mechanisms. We employed various assays, including the CCK-8 assay, flow cytometry, the Transwell and scratch assay, Western blotting, and nude mice transplantation tumor, to investigate the impact of KIF15 on NPC. Our findings demonstrate that KIF15 plays a critical role in the proliferation, apoptosis, migration, and invasion of NPC cells. Furthermore, we discovered that silencing KIF15 inhibits cell proliferation, migration, and invasion while promoting apoptosis, and that KIF15's effect on NPC cell growth is mediated through the PI3K/AKT and P53 signaling pathways. Additionally, we showed that KIF15 promotes nasopharyngeal cancer cell growth in vivo. Our study sheds light on the significance of KIF15 in NPC by revealing that KIF15 knockdown inhibits NPC cell growth through the regulation of AKT-related signaling pathways. These findings suggest that KIF15 represents a promising therapeutic target for the prevention and treatment of NPC.