Kinesin superfamily member 15 knockdown inhibits cell proliferation, migration, and invasion in nasopharyngeal carcinoma
Yi Cai1,#, Qianyue Lai1,#, Xuan Zhang1,#, Yu Zhang1, Man Zhang1, Shaoju Gu2, Yuan Qin1,*, Jingshen Hou3,*, and Li Zhao1,*
1Guangzhou Municipal and Guangdong Provincial Key Laboratory of Molecular Target & Clinical Pharmacology, the NMPA and State Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou 511436, 2Laboratory Animal Centre, Guangzhou Medical University, Guangzhou 511436, 3The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou 510260, China
Author contributions: Y.C. and Q.L. performed the cell-based assay experiments. X.Z., Y.Z., M.Z., and S.G. performed the animal-based assay experiments. Y.Q., J.H., and L.Z. supervised and coordinated the study. Y.C., Q.L., and X.Z. wrote and revised the manuscript.
Received: April 12, 2023; Revised: June 20, 2023; Accepted: June 27, 2023
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
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.