KIF23 in disease pathogenesis and therapeutics : from molecular mechanisms to clinical translation

Kinesin family member 23 (KIF23), a key regulator of cell division, has attracted growing interest owing to its aberrant expression and functional dysregulation in numerous human diseases. However, its systematic mechanisms of action across various pathological types and its potential for clinical translation remain to be fully elucidated. This review integrates multidisciplinary literature and bioinformatics data to systematically summarize the molecular characteristics, regulatory networks, and core functions of KIF23 in various diseases. Accumulating evidence indicates that KIF23 is overexpressed in numerous malignant tumors, where it drives tumor proliferation, metastasis, and drug resistance by regulating cell cycle progression, the DNA damage response, metabolic reprogramming, and remodeling of the immune microenvironment. Its overexpression is strongly associated with poor prognoses. KIF23 also plays a significant role in various non-cancerous diseases, such as congenital dyserythropoietic anemia, pulmonary arterial hypertension, and neurocognitive disorders. Notably, it exhibits tumor-suppressive effects in specific contexts, including cervical cancer, highlighting its context-dependent function. Preclinical evidence indicates that targeting KIF23 effectively suppresses tumor progression and reverses drug resistance. In conclusion, preclinical evidence suggests that KIF23 is a molecule with significant translational potential, demonstrating promising prospects in disease diagnosis, prognostic assessment, and targeted therapy. Further in-depth research on KIF23 will significantly advance precision medicine.