KIF3A inhibits nasopharyngeal carcinoma proliferation, migration and invasion by interacting with β-catenin to suppress its nuclear accumulation

作者：Hu, Zhe; Meng, Jinlan; Cai, Hongbing; Ma, Na; Gao, Xiujie; Li, Xiaojuan; Xu, Yan^*

来源：American Journal of Cancer Research, 2022, 12(11): 5226-5240.

• Nasopharyngeal carcinoma
• kinesin family member 3A
• proliferation
• migration

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 on-cogenesis 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 pro-liferation, migration, and invasion. Mechanistic studies found that KIF3A bound beta-catenin and attenuated beta-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 beta-catenin. Taken together, our data suggest that KIF3A interacts with beta-catenin and attenuates NPC proliferation, migration, and invasion by suppressing the intra-nuclear aggregation of beta-catenin. KIF3A may be a promising therapeutic target of patients with NPC.

• 单位
  广东药学院; y; 南方医科大学