ArticleThe EMBO journal2024
Weakened APC/C activity at mitotic exit drives cancer vulnerability to KIF18A inhibition.
Article in The EMBO journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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Who cites it
22 citing papers in PubMed, 25 citations in OpenAlex.
- KIF18A inhibitor prevents chromosomally unstable osteosarcoma growth by activating spindle assembly checkpoint.Cancer biology & therapy · 2026Article
- Chromosomal instability in cancer: sources, consequences and new therapeutic opportunities.Signal transduction and targeted therapy · 2026Review
- A bioinformatics analysis of KIF transcriptomic subtyping reveals prognostic heterogeneity and differential therapeutic responses in cervical cancer.Oncology letters · 2026Article
- Spindle Assembly Checkpoint Competency Determines Sensitivity to KIF18A Inhibition in Small Cell Lung Cancer.Cancer research communications · 2026Article
- The DNA damage response pathway is required for multiciliated cell differentiation.Current biology : CB · 2026Article
- KIF18A Maintains Kinetochore-Microtubule Attachments in CIN Cells by Limiting Microtubule Polymerization.bioRxiv : the preprint server for biology · 2026Article
- Impact of Chromosomal Instability and Aneuploidy in Cancer Development.Annual review of cancer biology · 2026Article
- Biological clocks keep a watch on mitosis.Nature cell biology · 2026Review
- Article
- KIF18A promotes chromosome congression in cooperation with CENP-E downstream of CENP-C.Cell reports · 2025Article
- Modeling and targeting general and chromosome-specific aneuploidy in cancer.Genes & development · 2025Review
- Anapc5 and Anapc7 as genetic modifiers of KIF18A function in fertility and mitotic progression.Scientific reports · 2025Article
- Centriole structural integrity defects are a crucial feature of hydrolethalus syndrome.The Journal of cell biology · 2025Article
- Chromosomal Instability and Clonal Heterogeneity in Breast Cancer: From Mechanisms to Clinical Applications.Cancers · 2025Review
- Targeting Kinesins for Therapeutic Exploitation of Chromosomal Instability in Lung Cancer.Cancers · 2025Review
- Small Molecules Identified by an In Silico Docking Screen Targeting Anaphase-Promoting Complex/Cyclosome Subunit 1 (APC1) Potentiate Paclitaxel-Induced Breast Cancer Cell Death.Molecules (Basel, Switzerland) · 2025Article
- Targeting chromosomally unstable tumors with a selective KIF18A inhibitor.Nature communications · 2025Article
- KIF18A induces the EMT process of hepatoma cells through the 5-LOX-dependent arachidonic acid pathway.PloS one · 2025Article
- Microtubule poleward flux as a target for modifying chromosome segregation errors.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Maternal genetic variants in kinesin motor domains prematurely increase egg aneuploidy.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 2 countries.
Funding
Abstract
The efficacy of current antimitotic cancer drugs is limited by toxicity in highly proliferative healthy tissues. A cancer-specific dependency on the microtubule motor protein KIF18A therefore makes it an attractive therapeutic target. Not all cancers require KIF18A, however, and the determinants underlying this distinction remain unclear. Here, we show that KIF18A inhibition drives a modest and widespread increase in spindle assembly checkpoint (SAC) signaling from kinetochores which can result in lethal mitotic delays. Whether cells arrest in mitosis depends on the robustness of the metaphase-to-anaphase transition, and cells predisposed with weak basal anaphase-promoting complex/cyclosome (APC/C) activity and/or persistent SAC signaling through metaphase are uniquely sensitive to KIF18A inhibition. KIF18A-dependent cancer cells exhibit hallmarks of this SAC:APC/C imbalance, including a long metaphase-to-anaphase transition, and slow mitosis overall. Together, our data reveal vulnerabilities in the cell division apparatus of cancer cells that can be exploited for therapeutic benefit.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.