Kif3a, a member of the kinesin-2 family, is a microtubule-oriented motor protein. It is crucial for regulating intracellular transport and microtubule movement, and is associated with pathways like the Wnt/β-catenin pathway [4]. It plays an overall significant role in various biological processes such as cell cycle regulation, organelle distribution, and ciliogenesis [1,5,6]. Genetic models, especially KO/CKO mouse models, have been valuable in studying its functions.

In mouse oocyte meiosis, conditional knockout of Kif3a leads to maturation defects, spindle assembly abnormalities, and organelle distribution disorders. It activates the spindle assembly checkpoint, causing metaphase I arrest. Kif3a depletion also results in aberrant spindle pole organization and reduced microtubule stability [1]. In nasopharyngeal carcinoma (NPC) stem cells, knocking down the Kif3a gene reduces cell vitality and inhibits the malignant phenotype by suppressing HIF-1 and NF-κB expression [2]. Overexpression of Kif3a in NPC cells inhibits proliferation, migration, and invasion by interacting with β-catenin to suppress its nuclear accumulation [3]. In Eriocheir sinensis spermatogenesis, knocking down es-kif3a decreases the expression of es-β-catenin and es-dvl, and changes the location of Es-β-catenin from the nucleus to the cytoplasm [4].

In conclusion, Kif3a is essential for multiple biological functions including meiotic progression, cell cycle regulation, and organelle distribution. Mouse KO/CKO models have revealed its significant roles in oocyte meiosis and in cancer-related processes such as in NPC, providing insights into disease mechanisms and potential therapeutic targets.