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Yi Cai,Qianyue Lai,Xuan Zhang,Yu Zhang,Man Zhang,Shaoju Gu,Yuan Qin,Jingshen Hou,Li Zhao 대한약리학회 2023 The Korean Journal of Physiology & Pharmacology Vol.27 No.5
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. INTRODUCTION Nasopharyngeal carcinoma (NPC), a malignant epithelial tumor, typically arises in the top and lateral walls of the nasopharyngeal cavity and can invade surrounding tissues. It is a prevalent malignancy in China and exhibits a geographically uneven distribution [1]. Specifically, 92% of new cases occur in economically less developed countries, with at least twice as many new cases occurring in East or Southeast Asia [2]. The World Health Organization
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