Nasopharyngeal carcinoma (NPC) is a malignant epithelial tumor prevalent in southern China and Southeast Asia. Previous studies have shown that Kinesin Family Member 3A (KIF3A) plays a critical role in the oncogenesis of various cancer types. However, the role of KIF3A in NPC tumorigenesis and the mechanism underlying its function have not been reported. In this study, we found that KIF3A was significantly downregulated in NPC cells and tissues, and KIF3A expression in NPC patients was associated with tumor stage and was positively corrected with overall survival. In vitro and in vivo experiments indicated that overexpression of KIF3A inhibited NPC cell proliferation, migration, and invasion. Mechanistic studies found that KIF3A bound β-catenin and attenuated β-catenin aggregation in the nucleus. Moreover, rescue experiments demonstrated that the inhibitory effect of KIF3A on NPC proliferation, migration and invasion was partially dependent on β-catenin. Taken together, our data suggest that KIF3A interacts with β-catenin and attenuates NPC proliferation, migration, and invasion by suppressing the intranuclear aggregation of β-catenin. KIF3A may be a promising therapeutic target of patients with NPC.
