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Published on: September 14, 2010
KIF23 in disease pathogenesis and its therapeutic and diagnostic potential
Chunmiao Luo1, Fuxing Qin2, Dunwei Yao1
1Department of Gastroenterology, Baise People's Hospital, Baise, Guangxi, China.
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.
Insights
Kinesin family member 23 (KIF23) is vital for cell division and transport. Its dysregulation drives cancer and developmental disorders, highlighting its dual role and potential as a therapeutic target.
Area of Science:
- Molecular Biology
- Cell Biology
- Genetics
Background:
- Kinesin family member 23 (KIF23) is a motor protein crucial for cytokinesis, organelle transport, and signaling.
- KIF23 dysregulation is implicated in tumorigenesis and non-malignant disorders.
Purpose of the Study:
- To provide a comprehensive review of KIF23's mechanistic and translational insights in disease pathogenesis.
- To integrate recent findings on KIF23's role in both cancer and non-neoplastic conditions.
Main Methods:
- Literature search across major databases (PubMed, Web of Science, Embase, TCGA).
- Keywords: "KIF23," "MKLP1," "cytokinesis."
- Summarized bioinformatic findings, including pan-cancer screening and machine learning analyses.
Main Results:
- KIF23 is upregulated in cancers (colorectal, gastric, hepatocellular, breast), activating oncogenic pathways (Wnt/β-catenin, PI3K-Akt, NF-κB) and correlating with poor prognosis.
- Loss-of-function mutations cause non-neoplastic diseases (e.g., congenital dyserythropoietic anemia type III, primary microcephaly) due to cytokinesis failure.
- KIF23 expression is regulated by transcriptional, epigenetic, and ceRNA mechanisms; it shows potential as a diagnostic biomarker and therapeutic target.
Conclusions:
- KIF23 exhibits a context-dependent, dual role in disease, making it a target for precision medicine.
- Future research should explore splice variants, develop tumor-selective inhibitors, and validate biomarker panels for clinical translation.
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