Nasopharyngeal carcinoma (NPC) is a common malignant carcinoma of the head and neck

and the biological mechanisms underlying the pathogenesis of NPC remain not fully understood. In the present study

we systematically analyzed four independent NPC transcriptomic datasets and focused on identifying the critical molecular networks and novel key hub genes implicated in NPC. We found totally 170 common overlapping differentially expressed genes (DEGs) in the four NPC datasets. GO and KEGG pathway analysis revealed that cell cycle dysregulation is a critical event in NPC. Protein–protein interaction (PPI) network analysis identified a 15 hub-gene core network with overexpressed kinesin family member 2C (KIF2C) as a central regulator. Loss-of-function study demonstrated that knockdown of KIF2C significantly inhibited cell growth and cell motility

and delayed cell cycle progression

accompanied with dramatic mitotic defects in spindle formation in NPC cells. RNA-seq analysis revealed that KIF2C knockdown led to deregulation of various downstream genes. KIF2C could also regulate the AKT/mTOR pathways

and enhance paclitaxel sensitivity in NPC cells. Taken together

our results suggest that cell cycle dysregulation is a critical event during NPC pathogenesis and KIF2C is a novel key mitotic hub gene with therapeutic potential in NPC.