ArticleFrontiers in genetics2021
Mutation and Copy Number Alterations Analysis of KIF23 in Glioma.
Article in Frontiers in genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- KIF23 in disease pathogenesis and therapeutics : from molecular mechanisms to clinical translation.Cancer cell international · 2026Review
- KIF23 in disease pathogenesis and its therapeutic and diagnostic potential.Discover oncology · 2026Review
- KIF23 Overexpression Promotes Cell Viability, Migration, and Invasion via the Wnt/β-Catenin Signaling Pathway in Anaplastic Thyroid Carcinoma.International journal of endocrinology · 2026Article
- The midbody and midbody remnant: from cellular debris to signaling organelle with diagnostic and therapeutic potential.Molecular biology of the cell · 2025Review
- Decoding the Role of Kinesin Superfamily Proteins in Glioma Progression.Journal of molecular neuroscience : MN · 2025Review
- Bioinformatics Analysis Screening and Identification of Key Biomarkers and Drug Targets in Human Glioblastoma.Current medicinal chemistry · 2025Article
- Article
- ESPL1 is Elevated in Hepatocellular Carcinoma and Predicts Prognosis.International journal of general medicine · 2022Article
- Systematic Pan-Cancer Analysis of KIF23 and a Prediction Model Based on KIF23 in Clear Cell Renal Cell Carcinoma (ccRCC).Pharmacogenomics and personalized medicine · 2021Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In glioma, kinesin family member 23 (KIF23) is up-regulated and plays a vital role in oncogenesis. However, the mechanism underlying KIF23 overexpression in malignant glioma remains to be elucidated. This study aims to find potential causes of KIF23 high expression at genome level. To clarify this issue, we obtained point mutation and copy number alterations (CNAs) of KIF23 in 319 gliomas using whole-exome sequencing. Only two glioma samples with missense mutations in KIF23 coding region were identified, while 7 patients were detected with amplification of KIF23. Additional analysis showed that KIF23 amplification was significantly associated with higher expression of KIF23. Gene ontology analysis indicated that higher copy number of KIF23 was associated TNF-α signaling pathway and mitotic cell circle checkpoint, which probably caused by subsequent upregulated expression of KIF23. Moreover, pan-cancer analysis showed that gaining of copy number was significantly associated with higher expression of KIF23, consolidating our findings in glioma. Thus, it was deduced that elevated KIF23 expression in glioma tended to be caused by DNA copy number amplification, instead of mutation.
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Registered trials
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