KIF23 in disease pathogenesis and its therapeutic and diagnostic potential.

BACKGROUND

Kinesin family member 23 (KIF23) is a microtubule-dependent motor protein essential for cytokinesis, organelle transport, and signaling pathway regulation. Its dysregulation contributes to both tumorigenesis and non-malignant disorders; however, a comprehensive review integrating recent mechanistic and translational insights is currently lacking.

METHODS

A literature search across PubMed, Web of Science, Embase, and public databases (such as TCGA), using keywords including "KIF23," "MKLP1," and "cytokinesis" was performed. Published bioinformatic findings, including pan cancer screening and machine learning analyses, linking KIF23 to disease pathogenesis were summarized.

RESULTS

KIF23 is frequently upregulated in various cancers, such as colorectal, gastric, hepatocellular and breast cancer, where it activates key oncogenic pathways including Wnt/β-catenin, PI3K-Akt and NF-κB. It remodels the tumor immune microenvironment and correlates with poor prognosis. In contrast, loss-of-function mutations in KIF23 underlie several non-neoplastic diseases, such as congenital dyserythropoietic anemia type III and primary microcephaly, by causing cytokinesis failure and developmental defects. KIF23 expression is regulated through multilayered networks involving transcriptional, epigenetic and competing endogenous RNA (ceRNA) mechanisms. Preclinical studies underscore its potential as a diagnostic biomarker and a promising therapeutic target.

CONCLUSIONS

KIF23 plays a context-dependent, dual role in disease pathogenesis and represents a compelling target for precision medicine. Future research should focus on deciphering the functional heterogeneity of its splice variants, developing tumor-selective inhibitors and validating integrated biomarker panels to advance clinical translation.